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Olatoye FJ, Akindele AJ, Balogun OE, Awodele O, Adejare AA. Antihypertensive Effect of Kolaviron, a Bioflavonoid From Garcinia kola, in L-NAME Induced Hypertension in Rats. Nat Prod Commun 2023. [DOI: 10.1177/1934578x221148608] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 03/12/2023] Open
Abstract
The antihypertensive effect of Kolaviron (KV) has been demonstrated in ethanol- and sucrose-model of hypertension in our previous studies. However, there remains a need to further confirm and validate this effect in other models of hypertension. This study was devised to appraise the antihypertensive action of KV in N(G)-nitro-L-arginine methyl ester (L-NAME) induced experimental format of hypertension. Thirty-six (36) male Wistar rats were divided into 6 groups of 6 animals each. Group I represents the control group while Group II animals received L-NAME 40 mg/kg only. Groups III to V animals received L-NAME 40 mg/kg and 50, 100, and 200 mg/kg KV, respectively. Group VI animals received L-NAME 40 mg/kg and 0.14 mg/kg Lisinopril (LIS). Treatment was done orally for 28 days after which blood pressure was determined via the invasive method. After this, vital organs and blood were retrieved for analysis. KV and LIS elicited significant contraction ( P < .01-.001) in blood pressure producing up to 27%, 24%, and 22% reduction in systolic blood pressure, diastolic blood pressure, and mean arterial pressure, respectively. In addition, KV elicited a notable rise ( P < .05-.001) in catalase, reduced glutathione, and superoxide dismutase in the blood and vital organs. Results from this study further demonstrate and confirm that KV possesses notable blood pressure-lowering effect possibly through its well-documented antioxidant effect. Additional studies are advocated to validate the results from this study and determine the precise mechanism for the antihypertensive action of KV.
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Affiliation(s)
- Francis J. Olatoye
- Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria
| | - Abidemi James Akindele
- Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria
| | - Okikioluwa E. Balogun
- Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria
| | - Olufunsho Awodele
- Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria
| | - Abdullahi A. Adejare
- Department of Physiology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria
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Olatoye FJ, Akindele AJ, Onwe S. Ameliorative effect of Kolaviron, an extract of Garcinia kola seeds, on induced hypertension. JOURNAL OF COMPLEMENTARY & INTEGRATIVE MEDICINE 2021; 19:37-46. [PMID: 33977689 DOI: 10.1515/jcim-2020-0354] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 09/14/2020] [Accepted: 01/08/2021] [Indexed: 12/12/2022]
Abstract
OBJECTIVES Early diagnosis and management of known cardiovascular disease risk attributes such as hypertension lessens morbidity and mortality as well as increase quality of life of patients. This present study was modelled to investigate the ameliorative effect of Kolaviron, an extract of Garcinia kola Heckel seeds, in ethanol- and sucrose-induced hypertension. METHODS Test animals were divided into six groups of six animals each for each hypertensive model. Animals were treated daily with distilled water (10 ml/kg); 35% ethanol (3 g/kg) or sucrose (5-7%); Kolaviron (50, 100 and 200 mg/kg) separately plus ethanol or sucrose and Amlodipine (0.14 mg/kg) separately plus ethanol or sucrose for 8 weeks. Systolic, diastolic and mean arterial pressures were determined using non-invasive BP system after 8 weeks. Blood was obtained for the assessment of biochemical parameters, lipid profile and antioxidant indices. Vital organs were collected for approximation of tissue antioxidant levels. RESULTS Results show that Kolaviron at various doses and Amlodipine significantly reduced (p<0.05-0.001) the elevated systolic, diastolic, and mean arterial pressures produced by ethanol and sucrose administration. Additionally, Kolaviron and Amlodipine significantly overturned (p<0.05-0.001) the reduction in GSH, SOD and CAT, and elevation in MDA levels elicited by ethanol and sucrose. Furthermore, Kolaviron and Amlodipine produced significant reduction (p<0.001) in levels of cholesterol, triglycerides and low-density lipoproteins, as well as significant increase (p<0.01-0.001) in levels of high-density lipoproteins. CONCLUSIONS Results from this study demonstrate that Kolaviron possibly possesses significant antihypertensive effect which may possibly be attributed to its antioxidant effects and relative improvement of lipid profile.
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Affiliation(s)
- Francis J Olatoye
- Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Lagos, Nigeria
| | - Abidemi J Akindele
- Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Lagos, Nigeria
| | - Samson Onwe
- Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Sciences, College of Medicine, University of Lagos, Lagos, Nigeria
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Abstract
Introduction: Despite the improved treatment protocol of hypertension, the magnitude of the disease and its related burden remains raised. Hypertension makes up the leading cause of stroke, kidney disease, arterial disease, eye disease, and cardiovascular disease (CVD) growth. Areas covered: This review provides the overview of the role of dietary salt and alcohol use reduction in the management of hypertension, a brief history of alcohol, the vascular endothelium functions, the effects of alcohol use on blood pressure (BP), the mechanisms of alcohol, brief history of salt, the effects of dietary salt intake on BP, and the mechanisms of salt. Expert opinion: Studies found that high dietary salt intake and heavy alcohol consumption have a major and huge impact on BP while both of them have been identified to increase BP. Also, they raise the risk of hypertension-related morbidity and mortality in advance. On the other way, the dietary salt and alcohol use reduction in the management of hypertension are significant in the control of BP and its related morbidity and mortality. Further, studies suggested that the dietary salt and alcohol use reductions are the cornerstone in the management of hypertension due to their significance as part of comprehensive lifestyle modifications.
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Affiliation(s)
- Addisu Dabi Wake
- Nursing Department, College of Health Sciences, Arsi University , Asella, Ethiopia
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Abstract
OBJECTIVE To assess the prevalence of metabolic syndrome (MetS) in Chinese adults living in Ningbo and to examine the association between alcohol consumption and MetS and its medical components. DESIGN A representative survey in Ningbo was conducted in 2015 covering socio-demography. A FFQ together with additional questionnaires was used to collect information on alcohol consumption, diet, demography, lifestyle and medical information. Multivariable logistic regression and generalised linear models were used to examine the association between alcohol consumption and both MetS and its medical components, respectively. SETTING Ningbo, China. PARTICIPANTS A total of 2853 adults ≥ 20 years (44 % men) in this final analysis. RESULTS The prevalence of frequent alcohol drinkers and MetS was 29·9 % and 28·0 %, respectively. Significantly higher prevalence of MetS and mean values of medical components were found in the group of frequent alcohol drinkers with an exception for HDL-cholesterol, compared with less or non-alcohol drinkers. Frequent alcohol consumption was associated with higher odds of developing MetS and positively associated with medical components excepting waist circumference. CONCLUSIONS Frequent alcohol consumption contributed to a higher prevalence of MetS and unfavourable influence on MetS and its medical components among Chinese adults. A public health intervention on alcohol restriction is necessary for the prevention and control of the ongoing epidemic MetS.
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Choi S, Kim K, Lee JK, Choi JY, Shin A, Park SK, Kang D, Park SM. Association between Change in Alcohol Consumption and Metabolic Syndrome: Analysis from the Health Examinees Study. Diabetes Metab J 2019; 43:615-626. [PMID: 31237129 PMCID: PMC6834843 DOI: 10.4093/dmj.2018.0128] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/18/2018] [Accepted: 12/02/2018] [Indexed: 01/12/2023] Open
Abstract
BACKGROUND The association between change in alcohol intake and metabolic syndrome is unclear. METHODS This retrospective cohort consisted of 41,368 males and females from the Health Examinees-GEM study. Participants were divided into non-drinkers (0.0 g/day), light drinkers (male: 0.1 to 19.9 g/day; female: 0.1 to 9.9 g/day), moderate drinkers (male: 20.0 to 39.9 g/day; female: 10.0 to 19.9 g/day), and heavy drinkers (male: ≥40.0 g/day; female: ≥20.0 g/day) for each of the initial and follow-up health examinations. Logistic regression analysis was used to determine the adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for developing metabolic syndrome according to the change in alcohol consumption between the initial and follow-up health examinations. Adjusted mean values for the change in waist circumference, fasting serum glucose (FSG), blood pressure, triglycerides, and high density lipoprotein cholesterol (HDL-C) levels were determined according to the change in alcohol consumption by linear regression analysis. RESULTS Compared to persistent light drinkers, those who increased alcohol intake to heavy levels had elevated risk of metabolic syndrome (aOR, 1.45; 95% CI, 1.09 to 1.92). In contrast, heavy drinkers who became light drinkers had reduced risk of metabolic syndrome (aOR, 0.61; 95% CI, 0.44 to 0.84) compared to persistent heavy drinkers. Increased alcohol consumption was associated with elevated adjusted mean values for waist circumference, FSG, blood pressure, triglycerides, and HDL-C levels (all P<0.05). Reduction in alcohol intake was associated with decreased waist circumference, FSG, blood pressure, triglycerides, and HDL-C levels among initial heavy drinkers (all P<0.05). CONCLUSION Heavy drinkers who reduce alcohol consumption could benefit from reduced risk of metabolic syndrome.
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Affiliation(s)
- Seulggie Choi
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea
| | - Kyuwoong Kim
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea
| | - Jong Koo Lee
- Department of Family Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
- JW Lee Center for Global Medicine, Seoul, Korea
| | - Ji Yeob Choi
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
| | - Aesun Shin
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
| | - Sue Kyung Park
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
| | - Daehee Kang
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
- Department of Environmental Medicine, Seoul National University Medical Research Center, Seoul, Korea
| | - Sang Min Park
- Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea
- Department of Family Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.
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Kuntamallappanavar G, Dopico AM. BK β1 subunit-dependent facilitation of ethanol inhibition of BK current and cerebral artery constriction is mediated by the β1 transmembrane domain 2. Br J Pharmacol 2017; 174:4430-4448. [PMID: 28940182 DOI: 10.1111/bph.14046] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/16/2017] [Revised: 09/11/2017] [Accepted: 09/14/2017] [Indexed: 11/28/2022] Open
Abstract
BACKGROUND AND PURPOSE Ethanol at concentrations obtained in the circulation during moderate-heavy episodic drinking (30-60 mM) causes cerebral artery constriction in several species, including humans. In rodents, ethanol-induced cerebral artery constriction results from ethanol inhibition of large conductance voltage/Ca2+i -gated K+ (BK) channels in cerebral artery myocytes. Moreover, the smooth muscle-abundant BK β1 accessory subunit is required for ethanol to inhibit cerebral artery myocyte BK channels under physiological Ca2+i and voltages and thus constrict cerebral arteries. The molecular bases of these ethanol actions remain unknown. Here, we set to identify the BK β1 region(s) that mediates ethanol-induced inhibition of cerebral artery myocyte BK channels and eventual arterial constriction. EXPERIMENTAL APPROACH We used protein biochemistry, patch-clamp on engineered channel subunits, reversible cDNA permeabilization of KCNMB1 K/O mouse arteries and artery in vitro pressurization. KEY RESULTS Ethanol inhibition of BK current was facilitated by β1 but not β4 subunits. Furthermore, only BK complexes containing β chimeras with β1 transmembrane (TM) domains on a β4 background or with a β1 TM2 domain on a β4 background displayed ethanol responses identical to those of BK complexes including wild-type β1. Moreover, β1 TM2 itself but not other β regions were necessary for ethanol-induced cerebral artery constriction. CONCLUSIONS AND IMPLICATIONS BK β1 TM2 is necessary for this subunit to enable ethanol-induced inhibition of myocyte BK channels and cerebral artery constriction at physiological Ca2+ and voltages. Thus, novel agents that target β1 TM2 may be considered to counteract ethanol-induced cerebral artery constriction and associated cerebrovascular conditions.
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Affiliation(s)
- Guruprasad Kuntamallappanavar
- Department of Pharmacology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, USA
| | - Alex M Dopico
- Department of Pharmacology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, USA
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Husain K, Ansari RA, Ferder L. Alcohol-induced hypertension: Mechanism and prevention. World J Cardiol 2014; 6:245-252. [PMID: 24891935 PMCID: PMC4038773 DOI: 10.4330/wjc.v6.i5.245] [Citation(s) in RCA: 189] [Impact Index Per Article: 17.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/28/2013] [Accepted: 04/16/2014] [Indexed: 02/06/2023] Open
Abstract
Epidemiological, preclinical and clinical studies established the association between high alcohol consumption and hypertension. However the mechanism through which alcohol raises blood pressure remains elusive. Several possible mechanisms have been proposed such as an imbalance of the central nervous system, impairment of the baroreceptors, enhanced sympathetic activity, stimulation of the renin-angiotensin-aldosterone system, increased cortisol levels, increased vascular reactivity due to increase in intracellular calcium levels, stimulation of the endothelium to release vasoconstrictors and loss of relaxation due to inflammation and oxidative injury of the endothelium leading to inhibition of endothelium-dependent nitric oxide production. Loss of relaxation due to inflammation and oxidative injury of the endothelium by angiotensin II leading to inhibition of endothelium-dependent nitric oxide production is the major contributors of the alcohol-induced hypertension. For the prevention of alcohol-induced hypertension is to reduce the amount of alcohol intake. Physical conditioning/exercise training is one of the most important strategies to prevent/treat chronic alcohol-induced hypertension on physiological basis. The efficacious pharmacologic treatment includes the angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (ARBs) which have antioxidant activity and calcium channel blockers. The most effective prevention and treatment of alcohol-induced hypertension is physical exercise and the use of ACE inhibitors or ARBs in the clinic
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Marchi KC, Muniz JJ, Tirapelli CR. Hypertension and chronic ethanol consumption: What do we know after a century of study? World J Cardiol 2014; 6:283-294. [PMID: 24944758 PMCID: PMC4062120 DOI: 10.4330/wjc.v6.i5.283] [Citation(s) in RCA: 63] [Impact Index Per Article: 5.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/18/2013] [Revised: 03/11/2014] [Accepted: 04/16/2014] [Indexed: 02/06/2023] Open
Abstract
The influences of life habits on the cardiovascular system may have important implications for public health, as cardiovascular diseases are among the leading causes of shorter life expectancy worldwide. A link between excessive ethyl alcohol (ethanol) consumption and arterial hypertension was first suggested early last century. Since then, this proposition has received considerable attention. Support for the concept of ethanol as a cause of hypertension derives from several epidemiologic studies demonstrating that in the general population, increased blood pressure is significantly correlated with ethanol consumption. Although the link between ethanol consumption and hypertension is well established, the mechanism through which ethanol increases blood pressure remains elusive. Possible mechanisms underlying ethanol-induced hypertension were proposed based on clinical and experimental observations. These mechanisms include an increase in sympathetic nervous system activity, stimulation of the renin-angiotensin-aldosterone system, an increase of intracellular Ca2+ in vascular smooth muscle, increased oxidative stress and endothelial dysfunction. The present report reviews the relationship between ethanol intake and hypertension and highlights some mechanisms underlying this response. These issues are of interest for the public health, as ethanol consumption contributes to blood pressure elevation in the population.
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Siervogel RM. Genetic and familial factors in essential hypertension and related traits. AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 2012. [DOI: 10.1002/ajpa.1330260504] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/08/2022]
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Movva R, Figueredo VM. Alcohol and the heart: to abstain or not to abstain? Int J Cardiol 2012; 164:267-76. [PMID: 22336255 DOI: 10.1016/j.ijcard.2012.01.030] [Citation(s) in RCA: 40] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/07/2011] [Revised: 01/07/2012] [Accepted: 01/19/2012] [Indexed: 12/12/2022]
Abstract
Alcohol has been consumed by most societies over the last 7000 years. Abraham Lincoln said "It has long been recognized that the problems with alcohol relate not to the use of a bad thing, but to the abuse of a good thing." Light to moderate alcohol consumption reduces the incidence of coronary heart disease (CHD), ischemic stroke, peripheral arterial disease, CHD mortality, and all-cause mortality, especially in the western populations. However, heavy alcohol consumption is detrimental causing cardiomyopathy, cardiac arrhythmias, hepatic cirrhosis, pancreatitis, and hemorrhagic stroke. In this article, we review the effects of alcohol on CHD, individual cardiovascular risk factors, cardiomyopathy, and cardiac arrhythmias, including the most recent evidence of the effects of alcohol on CHD.
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Affiliation(s)
- Rajesh Movva
- Albert Einstein Medical Center, Philadelphia, PA 19141, United States
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Soardo G, Donnini D, Moretti M, Milocco C, Catena C, Sechi LA. Effects of antihypertensive drugs on alcohol-induced functional responses of cultured human endothelial cells. Hypertens Res 2008; 31:345-51. [PMID: 18360055 DOI: 10.1291/hypres.31.345] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/07/2023]
Abstract
Alcohol-induced endothelial changes might contribute to an increase in blood pressure in regular alcohol consumers. Some antihypertensive drugs affect oxidative stress and endothelial function and might counteract the effects of alcohol at the cellular level. The aim of this study was to investigate in vitro the effects of three different types of antihypertensive agents on alcohol-induced endothelial responses and oxidative stress. Cultured human endothelial cells were exposed to increasing concentrations (1, 10, 60 micromol/L) of zofenoprilat, carvedilol, and lacidipine in the absence and in the presence of ethanol (140 mmol/L). Concentrations of endothelin (ET) and nitric oxide (NO) were measured in the culture media as markers of endothelial function, and malondialdehyde (MDA) and intracellular glutathione (GSHi) were measured as markers of oxidative stress. Exposure to alcohol increased the levels of ET, NO, and MDA, and decreased GSHi. Carvedilol and zofenoprilat were more effective than lacidipine in counteracting the effects of alcohol on ET production. Alcohol-induced NO production was enhanced by carvedilol, whereas zofenoprilat and lacidipine did not have a significant effect. The alcohol-induced increase in MDA concentrations was blunted by all three drugs, but only carvedilol restored a normal response. All three drugs increased GSHi levels, with the effect being greater for carvedilol and lacidipine than zofenoprilat. Carvedilol is more effective than zofenoprilat and lacidipine in counteracting alcohol-induced endothelial responses in vitro and in decreasing oxidative stress. These effects might be particularly beneficial in patients with alcohol-related hypertension.
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Affiliation(s)
- Giorgio Soardo
- Division of Internal Medicine-Liver Unit, Department of Experimental and Clinical Pathology and Medicine, University of Udine School of Medicine, Udine, Italy.
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Bär KJ, Boettger MK, Neubauer R, Grotelüschen M, Jochum T, Baier V, Sauer H, Voss A. Heart rate variability and sympathetic skin response in male patients suffering from acute alcohol withdrawal syndrome. Alcohol Clin Exp Res 2006; 30:1592-8. [PMID: 16930222 DOI: 10.1111/j.1530-0277.2006.00191.x] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/01/2022]
Abstract
BACKGROUND Many symptoms of alcohol withdrawal (AW) such as tachycardia or elevated blood pressure might be explained by increased peripheral and central adrenergic activity. In contrast to many neurochemical studies of sympathetic activation during AW, only very few studies investigated autonomic balance using neurophysiological methods. METHODS We investigated heart rate variability (HRV) and sympathetic skin response (SSR) in male patients suffering from mild AW syndrome (n = 20, no treatment required) and in patients with moderate to severe AW syndrome (n = 20, clomethiazole treatment) in the acute stage. Sympathovagal influence was quantified using measures of time and frequency domain of HRV as well as modern nonlinear parameters (compression entropy). Furthermore, we obtained latencies and amplitudes of SSR to quantify isolated sympathetic influence. Measures were obtained during the climax of withdrawal symptomatology before treatment, 1 day after climax, and shortly before discharge from hospital. Alcohol withdrawal scores were obtained and correlated to autonomic measures. RESULTS Ambulatory blood pressure and AW scores revealed characteristic withdrawal symptoms in both patient groups. Apart from the nonlinear parameter compression entropy, Hc, measures of HRV revealed no sign of autonomic dysfunction in contrast to the significantly increased heart rates at the time of admission. Latencies and amplitudes of SSR did not indicate any increase of sympathetic activity. A negative correlation was found between Hc and mental withdrawal symptoms. CONCLUSIONS We show here that classical measures for autonomic nervous system activity such as HRV and SSR are not suitable for describing the autonomic changes seen in acute AW, although a major role for the sympathetic nervous system has been proposed. This might be due to multiple dysregulation of metabolites in AWS or to subtle alcohol-induced damage to neuronal structures, issues that should be addressed in future studies.
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Affiliation(s)
- Karl-Jürgen Bär
- Department of Psychiatry, Friedrich-Schiller-University of Jena, Jena, Germany.
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Soardo G, Donnini D, Varutti R, Milocco C, Basan L, Esposito W, Casaccio D, Isola M, Soldano F, Sechi LA. Effects of alcohol withdrawal on blood pressure in hypertensive heavy drinkers. J Hypertens 2006; 24:1493-8. [PMID: 16877950 DOI: 10.1097/01.hjh.0000239283.35562.15] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/24/2022]
Abstract
BACKGROUND Epidemiological investigations have demonstrated a close association between heavy alcohol consumption and hypertension. The mechanisms of this association, however, remain elusive. We studied the effects of alcohol withdrawal on blood pressure, hormonal parameters, and circulating markers of endothelial activity. METHODS In 14 hypertensive heavy alcohol consumers (> 200 g/day) who agreed to participate in a hospital withdrawal programme we monitored, for 30 days, blood pressure, plasma levels of renin, aldosterone, cortisol, endothelin, and plasminogen activator inhibitor 1 (PAI-1), and urinary levels of catecholamines. Patients in the withdrawal group were compared with eight hypertensive heavy drinkers who refused to participate in the programme and maintained regular alcohol consumption and 11 normotensive teetotalers. RESULTS By the third day after withdrawal, blood pressure was significantly decreased and the normalization of levels was obtained in 13 of 14 patients by the end of the study. Alcohol withdrawal significantly decreased plasma aldosterone and cortisol levels, but did not affect levels of active renin and fractionated urinary catecholamines. At baseline, plasma endothelin and PAI-1 levels were significantly higher in alcoholic individuals than in teetotalers, and after the cessation of alcohol intake decreased progressively, reaching levels different from baseline within 1 week. A significant correlation was found between changes in endothelin and PAI-1, and blood pressure variations during alcohol abstinence that remained significant only for endothelin with the multivariate approach. CONCLUSION Hypertension is rapidly reversible in the majority of heavy drinkers after the withdrawal of alcohol consumption. In these patients, hypertension is associated with an increased release of endothelial factors that might contribute to the increase in blood pressure.
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Affiliation(s)
- Giorgio Soardo
- Department of Internal Medicine, Liver Unit, University of Udine School of Medicine, Udine, Italy.
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Puddey IB, Beilin LJ. Alcohol and Hypertension. Hypertension 2005. [DOI: 10.1016/b978-0-7216-0258-5.50135-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/20/2022]
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Kähkönen S. Mechanisms of cardiovascular dysregulation during alcohol withdrawal. Prog Neuropsychopharmacol Biol Psychiatry 2004; 28:937-41. [PMID: 15380854 DOI: 10.1016/j.pnpbp.2004.05.039] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 05/10/2004] [Indexed: 11/21/2022]
Abstract
Alcohol withdrawal (AW) is often accompanied by functional cardiovascular abnormalities which return to normal in few days. However, in some patients, they can predict future alterations in the cardiovascular system, even if they remain in abstinence. These changes are mediated by several central and peripheral mechanisms closely related to AW. The level of activation in the sympathetic nervous system is an important factor regulating the functioning of the cardiovascular system in AW directly and/or indirectly with L-type calcium channels and nitric oxide (NO). Other factors may contribute to cardiovascular alterations in AW including the renin-angiotensin-aldosterone system, vasopressin, cortisol and sodium sensitivity. Monitoring of the cardiovascular system is needed in patients undergoing treatment for AW. The patients with elevated systolic blood pressure (SBP) and diastolic blood pressure (DBP) after resolution of AW may require a fuller work-up of their cardiovascular system.
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Affiliation(s)
- Seppo Kähkönen
- BioMag Laboratory, Medical Engineering Centre, Helsinki University Central Hospital, P.O. Box 340, FIN-00029 HUS, Finland.
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Estruch R, Sacanella E, De la Sierra A, Aguilera MT, Antúnez E, Nicolás JM, Fernández-Solá J, Coca A, Urbano-Márquez A. Effects of Alcohol Withdrawal on 24 Hour Ambulatory Blood Pressure Among Alcohol-Dependent Patients. Alcohol Clin Exp Res 2003; 27:2002-8. [PMID: 14691389 DOI: 10.1097/01.alc.0000100944.02340.46] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]
Abstract
BACKGROUND Although epidemiologic studies have reported an association between alcohol intake and high blood pressure (BP), the results of intervention studies have shown inconsistent results. We embarked on a study to determine whether different subgroups of alcohol-dependent patients may be identified in relation to the effect of alcohol on BP. METHODS Fifty alcohol-dependent men (mean age, 41.4 years) received 0.4 g of ethanol per kilogram of body weight every 4 hr in 200 ml of orange juice during 24 hr and the same amount of orange juice without ethanol during another 24 hr. Twenty-four hour ambulatory BP monitoring was performed during ethanol and orange juice intakes, as was hormonal and biochemical analysis. RESULTS Thirty-five (75%) alcohol-dependent men were normotensive and 15 (30%) hypertensive. Eighteen (51%) normotensive and 12 (80%) hypertensive subjects showed a significant decrease in 24 hr mean BP after ethanol withdrawal (mean decrease of 8.4 mm Hg [95% confidence interval, -11.2 to -5.7] and 12.5 mm Hg [confidence interval, -16.2 to -8.8], respectively) and were considered as sensitive to alcohol. The remaining alcohol-dependent subjects were considered as resistant to alcohol. Normotensive subjects sensitive to ethanol showed a significantly greater left ventricular mass and a significantly lower ejection fraction than those normotensive patients whose BP did not change after ethanol withdrawal (both p < 0.01). CONCLUSIONS More than three fourths of the hypertensive and more than half of the normotensive alcohol-dependent patients showed sensitivity to the pressor effects of ethanol. Impairment also was observed in heart function in normotensive patients sensitive to the pressor effects of ethanol.
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Affiliation(s)
- Ramón Estruch
- Alcohol Unit, Department of Internal Medicine, Hospital Clínic, University of Barcelona, Institut de Investigacions Biomèdiques August Pi i Sunyer, Spain.
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Affiliation(s)
- R Wolf
- Department of Dermatology, Tel-Aviv Sourasky Medical Center, Ichilov Hospital, Israel
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Friedman HS. Cardiovascular effects of alcohol. RECENT DEVELOPMENTS IN ALCOHOLISM : AN OFFICIAL PUBLICATION OF THE AMERICAN MEDICAL SOCIETY ON ALCOHOLISM, THE RESEARCH SOCIETY ON ALCOHOLISM, AND THE NATIONAL COUNCIL ON ALCOHOLISM 1998; 14:135-66. [PMID: 9751945 DOI: 10.1007/0-306-47148-5_6] [Citation(s) in RCA: 17] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
The ingestion of one or two alcoholic drinks can affect heart rate, blood pressure, cardiac output, myocardial contractility, and regional blood flow. These actions generally are not clinically important. In the presence of cardiovascular disease, however, even such small quantities of alcohol might result in transient unfavorable hemodynamic changes. Moreover, alcohol abuse can produce cardiac arrhythmias, hypertension, cardiomyopathy, stroke, and even sudden death. In contrast, moderate alcohol use produces changes that have an overall favorable effect on atherosclerotic-related vascular diseases. Because cardiovascular disease due to atherosclerosis is the leading cause of death in Western society, this desirable effect of alcohol use outweighs its detrimental actions, resulting in favorable findings in population studies. Nevertheless, the body of evidence argues against encouraging alcohol use for its cardiovascular effects.
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Affiliation(s)
- H S Friedman
- Department of Medicine, Long Island College Hospital, Brooklyn, New York, USA
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20
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PUDDEY IANB, BEILIN LAWRENCEJ, RAKIC VALENTINA. Alcohol, hypertension and the cardiovascular system: a critical appraisal. Addict Biol 1997; 2:159-70. [PMID: 26735633 DOI: 10.1080/13556219772705] [Citation(s) in RCA: 23] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
Cross-sectional and longitudinal population studies have provided a considerable corpus of evidence for an inverse association between light to moderate alcohol intake and both coronary artery disease and stroke. The formulation of balanced public health advice on the basis of such studies, however, needs to take into account the full spectrum of the effects of alcohol on the cardiovascular system, particularly its equally well documented effect to increase level of blood pressure and prevalence of hypertension. In this review, the broader implications of the association of alcohol with hypertension are discussed, principally in the context of the effect of higher levels of alcohol consumption to increase ischaemic and haemorrhagic stroke, left ventricular hypertrophy, congestive cardiomyopathy, cardiac arrhythmia and sudden cardiac death.
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21
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Iwase S, Matsukawa T, Ishihara S, Tanaka A, Tanabe K, Danbara A, Matsuo M, Sugiyama Y, Mano T. Effect of oral ethanol intake on muscle sympathetic nerve activity and cardiovascular functions in humans. JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM 1995; 54:206-14. [PMID: 7490422 DOI: 10.1016/0165-1838(95)00022-p] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/25/2023]
Abstract
The aim of the present study was to clarify the acute effect of alcohol drinking on muscle sympathetic nerve activity and other cardiovascular variables in young healthy human volunteers. Seven volunteers (25.0 +/- 4.7 years in age, weighing 59.9 +/- 5.9 kg) were instructed to lay down on a bed, and muscle sympathetic nerve activity (MSNA) was microneurographically recorded from the tibial nerve, simultaneously with an electrocardiogram, blood pressure with Finapres and autosphygmomanometer, cardiac output by impedance cardiography, and skin blood flow by laser Doppler flowmetry. After a 1-h rest, the subjects drank alcohol (0.6 g/kg) and were remained in resting position for 105 min. Blood ethanol levels indicated that they were moderately intoxicated. Heart rate constantly increased until 30 min after the ingestion, and maintained a peak level. MSNA was slightly but significantly suppressed just after the ingestion, and was gradually enhanced until the end of the experiment, showing a significant difference from the control level until 40 min in burst rate and until 25 min in total MSNA after the ingestion. Blood pressure showed an abrupt and transient increase at first, then gradual decrease until 30 min after the ingestion, and maintenance of the resting level until the end of the experiment. Cardiac output showed no constant tendency and no significant differences after the ingestion with wide interindividual variation. Skin blood flow increased 15 min after the ingestion.(ABSTRACT TRUNCATED AT 250 WORDS)
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Affiliation(s)
- S Iwase
- Department of Autonomic and Behavioral Neurosciences, Nagoya University, Japan
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22
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Randin D, Vollenweider P, Tappy L, Jéquier E, Nicod P, Scherrer U. Suppression of alcohol-induced hypertension by dexamethasone. N Engl J Med 1995; 332:1733-7. [PMID: 7760888 DOI: 10.1056/nejm199506293322601] [Citation(s) in RCA: 112] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Abstract
BACKGROUND Alcohol consumption is associated with an increased incidence of hypertension and stroke, but the triggering mechanisms are unclear. In animals, alcohol causes activation of the sympathetic nervous system and also stimulates the release of corticotropin-releasing hormone (CRH), which has sympatho-excitatory effects when administered centrally. METHODS To determine whether alcohol evokes sympathetic activation and whether such activation is attenuated by the inhibition of CRH release, we measured blood pressure, heart rate, and sympathetic-nerve action potentials (using intraneural microelectrodes) in nine normal subjects before and during an intravenous infusion of alcohol (0.5 g per kilogram of body weight over a period of 45 minutes) and for 75 minutes after the infusion. Each subject received two infusions, one after the administration of dexamethasone (2 mg per day) and one after the administration of a placebo for 48 hours. RESULTS The infusion of alcohol alone evoked a marked (P < 0.001) and progressive increase in the mean (+/- SD) rate of sympathetic discharge, from 16 +/- 3 bursts per minute at base line to 30 +/- 8 bursts per minute at the end of the two-hour period. This sympathetic activation was accompanied during the second hour by an increase in mean arterial pressure of 10 +/- 5 mm Hg (P < 0.001). After the administration of dexamethasone, the alcohol infusion had no detectable sympathetic effect. The dexamethasone-induced suppression of sympathetic activation was associated with a decrease in mean arterial pressure of 7 +/- 6 mm Hg (P < 0.001) during the alcohol infusion and with suppression of the pressor effect during the second hour. CONCLUSIONS Alcohol induces pressor effects by sympathetic activation that appear to be centrally mediated. It is possible that these alcohol-induced hemodynamic and sympathetic actions could participate in triggering cardiovascular events.
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Affiliation(s)
- D Randin
- Department of Internal Medicine B. Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
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23
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Abstract
1. Regular alcohol consumption is a significant contributor to the prevalence of hypertension in drinking communities. 2. The effect is additive to that of obesity and is partly reversible over 2-4 weeks with moderation of ethanol intake. 3. In heavy drinkers acute alcohol withdrawal may lead to more blood pressure elevation following an initial depressor response. 4. Heavy drinking is also associated with an increased risk of haemorrhagic stroke and cardiomyopathy. 5. Lighter drinking habits appear to offer significant protection against ischaemic heart deaths and ischaemic strokes. 6. Antihypertensive drug treatment for alcohol related hypertension may mask some of the adverse cardiovascular effects of alcohol. 7. Arguments as to whether alcohol is a cause of essential hypertension are tautological, given the many reversible lifestyle factors now known to contribute to the rise in blood pressure with aging.
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Affiliation(s)
- L J Beilin
- Department of Medicine, University of Western Australia, Royal Perth Hospital
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24
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Abdel-Rahman AA. Differential effects of ethanol on baroreceptor heart rate responses of conscious spontaneously hypertensive and normotensive rats. Alcohol Clin Exp Res 1994; 18:1515-22. [PMID: 7695053 DOI: 10.1111/j.1530-0277.1994.tb01459.x] [Citation(s) in RCA: 18] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/26/2023]
Abstract
This study investigated the acute effects of ethanol (0.25, 0.5, or 1 g/kg, iv) on mean arterial pressure, heart rate, and gain of the baroreceptor reflex control of heart rate (BRS) in conscious spontaneously hypertensive rats (SHRs) and age-matched Wistar rats. BRS was substantially lower in the SHRs as compared with the Wistar rats when measured by phenylephrine (-0.95 +/- 0.16 vs. -2.02 +/- 0.22 beats/min/mm Hg) or nitroprusside (-1.90 +/- 0.2 vs -3.02 +/- 0.32 beats/min/mm Hg). None of the doses of ethanol influenced BRS in the SHR. In contrast, ethanol attenuated BRS in Wistar rats, but this effect was dependent on the dose used and the type of response. The lower doses attenuated the reflex tachycardic response, but had no effect on the reflex bradycardic response. On the other hand, the 1 g/kg dose of ethanol attenuated the reflex bradycardic but not the tachycardic response. Ethanol produced a pressor effect (15-25 mm Hg; 5-min duration), which was neither dose- nor strain-dependent. However, only in the SHR mean arterial pressure remained elevated (10-15 mm Hg above control) for 20 min in response to the 0.5 g/kg dose of ethanol, and its recovery coincided with the occurrence of a slowly developing negative chronotropic response. Ethanol produced a dose-related negative chronotropic effect in both strains of rats that was of longer duration in the SHR, particularly with the 1 g/kg dose. It is possible that the bradycardic effect of ethanol influenced negatively its pressor effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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Affiliation(s)
- A A Abdel-Rahman
- Department of Pharmacology, East Carolina University School of Medicine, Greenville, North Carolina
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25
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Thevananther S, Brecher AS. Interaction of acetaldehyde with plasma proteins of the renin-angiotensin system. Alcohol 1994; 11:493-9. [PMID: 7865150 DOI: 10.1016/0741-8329(94)90074-4] [Citation(s) in RCA: 26] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Abstract
Chronic alcohol abuse may lead to hypertension by stimulating the activity of the renin angiotensin system (RAS). While there are reports on the alcohol associated increase of angiotensin II in rats and increases of plasma renin activity in rats and human alcoholics, the exact mechanisms of stimulation of the RAS activity is not clear. This study provides evidence for a biochemical interaction of acetaldehyde, the primary oxidative metabolite of ethanol, upon bilaterally nephrectomized (NEPEX) rat plasma that contains significant quantities of angiotensinogen and lacks active renin. Rat plasma served as the source of renin in this study. Preincubation of NEPEX plasma with 0.2 M acetaldehyde at 4 degrees C for 2 h resulted in a 21% increase in the angiotensin I (A I) formation by the rat plasma renin and 27% increase in the A I formation by the trypsinized rat plasma renin. When the rat plasma which contains modest quantities of endogenous angiotensinogen in addition to renin was preincubated with 0.2 M acetaldehyde at 4 degrees C for 2 h, the rate of A I formation was increased by 10%. Equivalent amounts of ethanol did not modify the rate of A I generation when added to NEPEX plasma or rat plasma. These results suggest the possibility of a biochemical interaction of acetaldehyde with the renin substrate which may enhance the activity of the RAS cascade, thereby contributing to hypertension in chronic alcoholics.
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Affiliation(s)
- S Thevananther
- Department of Biological Sciences, Bowling Green State University, OH 43403
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26
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Wright JW, Harding JW. Brain angiotensin receptor subtypes in the control of physiological and behavioral responses. Neurosci Biobehav Rev 1994; 18:21-53. [PMID: 8170622 DOI: 10.1016/0149-7634(94)90034-5] [Citation(s) in RCA: 209] [Impact Index Per Article: 6.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/29/2023]
Abstract
This review summarizes emerging evidence that supports the notion of a separate brain renin-angiotensin system (RAS) complete with the necessary precursors and enzymes for the formation and degradation of biologically active forms of angiotensins, and several binding subtypes that may mediate their diverse functions. Of these subtypes the most is known about the AT1 site which preferentially binds angiotensin II (AII) and angiotensin III (AIII). The AT1 site appears to mediate the classic angiotensin responses concerned with body water balance and the maintenance of blood pressure. Less is known about the AT2 site which also binds AII and AIII and may play a role in vascular growth. Recently, an AT3 site was discovered in cultured neoblastoma cells, and an AT4 site which preferentially binds AII(3-8), a fragment of AII now referred to as angiotensin IV (AIV). The AT4 site has been implicated in memory acquisition and retrieval, and the regulation of blood flow. In addition to the more well-studied functions of the brain RAS, we review additional less well investigated responses including regulation of cellular function, the modulation of sensory and motor systems, long term potentiation, and stress related mechanisms. Although the receptor subtypes responsible for mediating these physiologies and behaviors have not been definitively identified research efforts are ongoing. We also suggest potential contributions by the RAS to clinically relevant syndromes such as dysfunctions in the regulation of blood flow and ischemia, changes in cognitive affect and memory in clinical depressed and Alzheimer's patients, and angiotensin's contribution to alcohol consumption.
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Affiliation(s)
- J W Wright
- Department of Psychology, Washington State University, Pullman 99164-4820
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27
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Wigle DA, Pang SC, Radakovic NN, Sarda IR, Watson JD, Roy RN, Flynn TG. Chronic ethanol ingestion modifies the renin-aldosterone axis independent of alterations in the regulation of atrial natriuretic peptide. Alcohol Clin Exp Res 1993; 17:841-6. [PMID: 8214424 DOI: 10.1111/j.1530-0277.1993.tb00851.x] [Citation(s) in RCA: 18] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/29/2023]
Abstract
Using an animal model, we have investigated the effects of chronic ethanol ingestion on the regulation of atrial natriuretic peptide (ANP) synthesis and release. Male Sprague-Dawley rats were maintained for 6 weeks on a liquid diet of ethanol (up to 20% v/v) as part of a 2% solution of calf milk replacer. Weight-matched controls received an equal volume of ethanol-free solution, and normal animals drank ad libitum. All animals received rat chow throughout the experiment. This model produced physiologically relevant levels of blood ethanol, as concentrations at the time of sacrifice were 171.98 +/- 39.26 mg/dl. Plasma renin activity was significantly elevated in response to ethanol treatment, whereas circulating aldosterone concentration was reduced. No alterations in the plasma or atrial tissue levels of ANP were evident, although we did observe a significant increase in the ventricular tissue levels of ANP from 45.1 to 71.8 ng/g as a consequence of ethanol treatment. Levels of both atrial and ventricular ANP mRNA were not different between alcohol-treated and liquid-restricted control animals, although both groups showed significant increases in the amount of transcript in comparison with rats drinking ad libitum. No significant increases in either arterial blood pressure or heart/body weight ratio were observed for ethanol-treated rats. These results suggest that modifications in the renin-aldosterone axis can occur independently of alterations in the regulation of ANP under the influence of chronic ethanol ingestion.
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Affiliation(s)
- D A Wigle
- Department of Anatomy, Queen's University, Kingston, Canada
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28
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Wigle DA, Pang SC, Sarda IR, Watson JD, Radakovic NN, Roy R, Flynn TG. Acute ethanol ingestion modifies the circulating plasma levels of atrial natriuretic peptide. Alcohol 1993; 10:275-80. [PMID: 8397878 DOI: 10.1016/0741-8329(93)90005-9] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2023]
Abstract
Since ethanol ingestion is associated with a disruption of water and electrolyte balance in a variety of species, we sought to evaluate the regulatory control of atrial natriuretic peptide (ANP) in response to acute doses of ethanol. Male Sprague-Dawley rats were administered a 5-g/kg dose of ethanol (40% w/v) via a gastric tube, while control animals received an equivalent volume of water. Expressed as a percentage of control, plasma ANP levels were 39.0%, 28.5%, and 23.6% in the ethanol-treated animals at 30, 60, and 120 min postintubation, respectively. Ethanol-treated animals displayed blood alcohol concentrations of 89.0, 137.6, and 214.1 mg/dl at the same time periods. After 120 min, plasma renin activity was elevated from 8.7 to 20.3 ng/ml/h in conjunction with an increase in the levels of circulating aldosterone from 16.3 to 42.5 ng/dl and an increase in plasma vasopressin from 2.2 to 3.6 pg/ml. Levels of atrial ANP mRNA remained consistent over the time course of the experiment, and no changes in the amount of ventricular ANP transcript were observed. Tissue ANP levels were similar between ethanol-treated and water-loaded control animals. In vitro experiments using cultured cardiac myocytes suggest that ethanol exposure may not directly affect ANP secretion. We propose that acute ethanol treatment may inhibit atrial distension and subsequently modify the control of ANP release under volume loading conditions.
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Affiliation(s)
- D A Wigle
- Department of Anatomy, Queen's University, Kingston, Canada
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29
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Affiliation(s)
- L J Beilin
- University Department of Medicine, Royal Perth Hospital, Australia
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30
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Beilin LJ, Puddey IB. Alcohol and hypertension. CLINICAL AND EXPERIMENTAL HYPERTENSION. PART A, THEORY AND PRACTICE 1992; 14:119-38. [PMID: 1541032 DOI: 10.3109/10641969209036176] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
The relationship between regular alcohol consumption and blood pressure elevation is now firmly established. Outstanding issues which will be discussed relate to the nature of the dose response curve, interactions between alcohol and other dietary and behavioural factors, mechanisms involved and the question of any protective influence of alcohol on atherosclerotic and ischaemic cardiovascular disease associated with hypertension. Alcohol is an important contributory to the prevalence of hypertension, and resistance to drug therapy in drinking communities. Heavy drinking and binge drinking increases the risk of stroke.
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Affiliation(s)
- L J Beilin
- University Department of Medicine, Royal Perth Hospital, Western Australia
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31
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Russ R, Abdel-Rahman AR, Wooles WR. Role of the sympathetic nervous system in ethanol-induced hypertension in rats. Alcohol 1991; 8:301-7. [PMID: 1872991 DOI: 10.1016/0741-8329(91)90433-w] [Citation(s) in RCA: 49] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Abstract
The present study investigated the role of the sympathetic nervous system in the development of ethanol-induced hypertension (EIH) in the rat. Sympathetic nerve activity (SNA) as an index of central sympathetic tone was measured directly from the preganglionic fibers of the greater splanchnic nerve. Four weeks after starting ethanol feeding, and prior to the development of hypertension, SNA of the ethanol-fed rats was significantly greater than that of controls. The increase in SNA was also evident at the early stages of EIH, at 8 weeks, and in fully developed EIH, after 12 weeks of ethanol consumption. Baroreceptor reflex control of heart rate (HR) but not SNA was impaired prior to the development of EIH at 4 weeks. However, at 8 and 12 weeks, baroreflex control of HR and SNA was normal or slightly greater than that of control rats. Because arterial pressure of ethanol-fed rats was significantly higher than that of controls at 8 and 12 weeks, the data suggest that ethanol feeding caused baroreceptor resetting. Pressor responsiveness to phenylephrine was depressed before the development of EIH but was similar to that of control rats following the development of EIH. The data also shows that blood and plasma volumes of ethanol-fed rats at the times that coincided with the pre- and posthypertensive states were similar to those of control rats which suggests that the development of EIH does not involve an increase in plasma volume. It is concluded that an increase in SNA contributes to the development of EIH and that baroreceptor resetting evoked by ethanol feeding plays a permissive role in maintaining an elevated blood pressure in ethanol-fed rats.
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Affiliation(s)
- R Russ
- Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858
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32
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Potter JF, Beevers DG. Factors determining the acute pressor response to alcohol. CLINICAL AND EXPERIMENTAL HYPERTENSION. PART A, THEORY AND PRACTICE 1991; 13:13-34. [PMID: 1673650 DOI: 10.3109/10641969109082612] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Abstract
The pressor response to acute alcohol loading is variable and the factors influencing it are unknown. Data from 34 standardized alcohol loading studies were analysed to try to identify any factor(s) that might predict the pressor response to oral alcohol. The maximum blood pressure rise following an acute alcohol load was assessed for each subject over a 4 hour period. Age, weight, recent alcohol intake, baseline blood pressure, pulse rate and serum gamma glutamyl transferase levels were entered, as the independent variables, into a multiple linear regression analysis with the maximum blood pressure response as the dependent variable. Alcohol consumption in the week prior to the study predicted the systolic blood pressure pressor response to acute alcohol loading. None of the independent variables entered had any predictive value for diastolic or mean arterial blood pressure response.
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Affiliation(s)
- J F Potter
- University Department of Medicine for the Elderly, Leicester General Hospital, U.K
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33
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Howes LG, Krum H, Phillips PA. Effects of regular alcohol consumption on 24 hour ambulatory blood pressure recordings. Clin Exp Pharmacol Physiol 1990; 17:247-50. [PMID: 2347115 DOI: 10.1111/j.1440-1681.1990.tb01315.x] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
1. Regular consumption of 1 g/kg of alcohol for 4 days did not significantly alter mean 24 h blood pressures compared with a similar period when dextrose was consumed to match caloric intake. 2. In contrast, the variability of diastolic blood pressure was increased by regular alcohol consumption. 3. Increased blood pressure variability in response to the stress of blood pressure measurement may contribute to the observed association between hypertension and alcohol consumption.
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Affiliation(s)
- L G Howes
- University of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Vic., Australia
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34
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Woolf PD, Cox C, Kelly M, McDonald JV, Hamill RW. Alcohol intoxication blunts sympatho-adrenal activation following brain injury. Alcohol Clin Exp Res 1990; 14:205-9. [PMID: 2190486 DOI: 10.1111/j.1530-0277.1990.tb00473.x] [Citation(s) in RCA: 24] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
Abstract
In 46 patients experiencing traumatic brain injury, we studied the interactions of alcohol intoxication and severity of neurologic dysfunction on the resulting sympathetic nervous system activation. Sixty percent of the variation in norepinephrine (p less than 0.0001) and more than 50% of the variation in epinephrine (p less than 0.0001) were due to the initial ethanol concentrations and extent of brain injury assessed by the admission Glasgow Coma Score (GCS). As brain function deteriorated plasma cathecholamines rose (p less than 0.0001), but ethanol qualitatively and quantitatively modified this observation. The magnitude of the sympathetic response to worsening neurologic function was progressively diminished in association with increasing ethanol levels, i.e., the inverse relationship of GCS values with both norepinephrine and epinephrine was flattened. In comatose patients (GCS less than 8) increasing ethanol levels was associated with progressively decreasing norepinephrine and epinephrine responses (p less than 0.04), such that catecholamines were reduced by 80 to 90% at ethanol concentrations approaching 400 mg/dl (87.0 mmol/l). However, the impact of ethanol on the degree of sympathetic nervous system activation depended upon the degree of injury; the apparent ethanol suppression was greatest in patients with the most severe neurologic dysfunction (GCS 3 or 4), but it diminished as neurologic function improved. We conclude that the presence of alcohol appears to modify the rise in catecholamine levels following traumatic brain injury in a dose-dependent manner and alters the relationship between neurologic dysfunction and SNS activation. These alterations may have profound effects on patient morbidity in the immediate post-accident period.
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Affiliation(s)
- P D Woolf
- Department of Medicine, University of Rochester Medical Center, New York
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35
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Strickland JA, Wooles WR. Blood ethanol level and physiologic measurements during ethanol-induced hypertension. Alcohol 1989; 6:109-14. [PMID: 2540763 DOI: 10.1016/0741-8329(89)90034-7] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
Plasma norepinephrine levels and alpha 2-adrenoceptor binding in central nervous system areas involved in blood pressure regulation were determined during the development of ethanol-induced hypertension in rats. Blood pressure was increased after the 4th week of ethanol feeding. Plasma norepinephrine levels of the ethanol-fed group were lower than those of the control group at most time periods studied even though blood pressure was elevated. 3H-Clonidine binding to alpha 2-adrenoceptors was decreased in the anterior and posterior hypothalamus of ethanol-fed rats throughout most of the study. Blood pressure in the ethanol-fed group was elevated when blood ethanol concentration was high, whereas blood pressure in this group was similar to that of the control group when blood ethanol concentration was low. Brain and plasma samples were taken during low blood ethanol which may explain the lack of positive findings. These results suggest that ethanol is a pressor agent and must be present to exert its cardiovascular effects. These findings suggest the importance of blood ethanol concentration at the time of study and also suggest that the blood pressure elevating effects of ethanol may be central rather than peripheral in origin.
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Affiliation(s)
- J A Strickland
- Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858
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36
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Rhee HM, Valentine JL, Hendrix D, Schweisthal M, Soria M. Hemodynamic responses to vasoactive compounds in chronically alcohol treated rats. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY 1989; 248:629-39. [PMID: 2782179 DOI: 10.1007/978-1-4684-5643-1_70] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/02/2023]
Affiliation(s)
- H M Rhee
- Department of Pharmacology, Oral Roberts University, School of Medicine, Tulsa, OK 74137
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37
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Periti M, Salvaggio A, Quaglia G, Di Marzio L. Alcohol consumption and blood pressure. An Italian study. Eur J Epidemiol 1988; 4:477-81. [PMID: 3203730 DOI: 10.1007/bf00146402] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
We studied the relationship between alcohol consumption and arterial pressure in 1,190 subjects of both sexes aged between 18 and 63 years who were examined during the course of a program of preventive medicine organized by Centro Diagnostico Italiano. In 711 subjects who were not requested to alter their usual alcohol consumption we found a significant relationship between alcohol consumption and systolic arterial pressure, b + SE(b), 4.6 +/- 2.1 mmHg/100 g ethanol/day. In particular, males who were heavy drinkers (greater than or equal to 50 g ethanol/day) presented significantly higher systolic pressure levels than the other men, d +/- SE(d), 3.7 +/- 1.6 mmHg, whereas no significant differences were observed among the various classes of women subdivided according to alcohol intake (only 4.6% of the women consumed greater than 50 g ethanol/day). On the other hand, in 479 subjects who were requested to abstain from alcohol consumption during the three days preceding the examination, no significant relation was found between alcohol intake and arterial pressure. The difference between the systolic pressure levels of the male heavy drinkers and those of the male moderate and non-drinkers was only 0.1 mmHg. Excessive alcohol consumption, in this case, mainly in the form of wine, was therefore associated with higher systolic pressure levels. However, it seems that abstaining from alcohol for even a brief period may modify this relation considerably.
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Affiliation(s)
- M Periti
- Clinica Medica Generale Università degli Studi di Milano Ospedale L. Sacco, Milano, Italy
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38
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Strickland JA, Wooles WR. Effect of acute and chronic ethanol on the agonist responses of vascular smooth muscle. Eur J Pharmacol 1988; 152:83-91. [PMID: 3208835 DOI: 10.1016/0014-2999(88)90838-2] [Citation(s) in RCA: 38] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
We studied the effect of ethanol in vitro on the response of isolated rat aortas to phenylephrine and angiotensin II. We also examined the effect of chronic ethanol consumption on the phenylephrine response and the effect of ethanol in vitro on that response during the development of ethanol-induced hypertension. In acute experiments the depression of the phenylephrine dose-response produced by ethanol in vitro was greater than that for angiotensin II. Comparing the depression of these agonist dose-responses by ethanol to the depression by the receptor blockers, verapamil, prazosin and saralasin, suggests that ethanol may act like an alpha 1-adrenoceptor blocker. During chronic ethanol consumption two opposing changes occurred: (1) desensitization to phenylephrine during weeks 6-18 and, (2) tolerance to depression by ethanol in vitro during weeks 4-10. These opposing changes may cancel each other which suggests that the hypertension due to chronic ethanol consumption is probably not due to an action of ethanol on the vasculature.
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Affiliation(s)
- J A Strickland
- Department of Pharmacology, School of Medicine, East Carolina University, Greenville, North Carolina 27858
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Puddey IB, Jenner DA, Beilin LJ, Vandongen R. An appraisal of the effects of usual vs recent alcohol intake on blood pressure. Clin Exp Pharmacol Physiol 1988; 15:261-4. [PMID: 3271608 DOI: 10.1111/j.1440-1681.1988.tb01069.x] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/05/2023]
Abstract
1. In a population-based study of 343 men from two public utilities, 260 subjects reported drinking alcohol at least once a week. In these subjects a comparison was made of the relative effects on blood pressure of either their usual alcohol intake (assessed from a 7-day retrospective diary) or recent alcohol intake (alcohol consumed at the last drinking session in the 24 h prior to blood pressure measurement). 2. Both usual and recent alcohol intake showed similar correlations with level of blood pressure (BP). After adjustment of BP for the potential confounding influences of body mass index, age and smoking status, systolic and diastolic BP remained highest in those subjects with the highest reported levels of both usual and recent alcohol intake. 3. In regression analyses comprising only those subjects who reported drinking in the 24 h before BP measurement, a 3-4 fold greater effect of usual rather than recent intake on both systolic and diastolic BP was predicted from the b coefficients. Regression analysis also demonstrated that the relationship between usual alcohol intake and BP was independent of recent intake, while the relationship between recent intake and BP was no longer significant when usual alcohol intake was entered into the regression equation. 4. These observations suggest that consistent regular drinking is a more important determinant of the alcohol/BP relationship than intake in the previous 24 h.
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Affiliation(s)
- I B Puddey
- University of Western Australia Department of Medicine, Royal Perth Hospital
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Howes LG, Reid JL. Alcohol and hypertension. Scott Med J 1987; 32:6-8. [PMID: 3563479 DOI: 10.1177/003693308703200103] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/06/2023]
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Lang T, Degoulet P, Aime F, Devries C, Jacquinet-Salord MC, Fouriaud C. Relationship between alcohol consumption and hypertension prevalence and control in a French population. JOURNAL OF CHRONIC DISEASES 1987; 40:713-20. [PMID: 3597673 DOI: 10.1016/0021-9681(87)90108-1] [Citation(s) in RCA: 37] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/06/2023]
Abstract
Six thousand six hundred thirty two subjects, employed in 420 small and medium-sized companies in the Paris region were examined in a cross-sectional study. Their alcohol consumption, as obtained by interview was found to be higher among males than among females, among workers than among managers, executives, and clerks. Alcohol consumption was positively associated with age, body mass index, coffee and cigarette consumption, occupational exposure to noise and working nights or alternating shifts. A positive, continuous, relationship was observed, for men and women, between alcohol intake and both systolic and diastolic blood pressure. This association was highly significant in the multivariate analysis (multiple linear regression) where alcohol intake, following age and body mass index, was the third predictive factor of blood pressure level in the stepwise regression. The positive association between alcohol consumption and prevalence of arterial hypertension was aggravated by the poor control of hypertension which was found among drinkers. Awareness of hypertension, compliance with an antihypertensive treatment and its efficacy, were negatively associated with alcohol intake. The findings stress the importance of alcohol consumption which was found to be a major risk factor for arterial hypertension and noncompliance with antihypertensive treatment in this population.
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Johnson RH, Eisenhofer G, Lambie DG. The effects of acute and chronic ingestion of ethanol on the autonomic nervous system. Drug Alcohol Depend 1986; 18:319-28. [PMID: 3816527 DOI: 10.1016/0376-8716(86)90094-3] [Citation(s) in RCA: 51] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/07/2023]
Abstract
Evidence is reviewed linking clinical effects of ethanol with actions on the sympathetic and parasympathetic nervous systems. The studies reported include a series of investigations by the authors. Acutely, ethanol causes peripheral vasodilation and may also result in changes in heart rate and blood pressure. Ethanol may contribute to acute problems which may present clinically, including micturition syncope, accidental hypothermia and facial flushing. However, increased sympathetic nervous activity plays a role in causing hypertension and other symptoms during ethanol withdrawal in chronic alcoholics. Some chronic alcoholics may have neuropathy involving sympathetic nerves, and this can result in distal sweating loss and occasionally in orthostatic hypotension. Also, hypothalamic lesions associated with Wernicke's encephalopathy may result in hypothermia. Neuropathy involving parasympathetic nerves in not uncommon in alcoholics with other evidence of nervous system damage, but it is generally asymptomatic. Occasionally, vagal neuropathy may cause disorder of gastrointestinal motility, and neuropathy affecting the sacral innervation may be a factor in alcoholic impotence.
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Howes LG, MacGilchrist A, Hawksby C, Sumner D, Reid JL. Plasma [3H]-noradrenaline kinetics and blood pressure following regular, moderate ethanol consumption. Br J Clin Pharmacol 1986; 22:521-6. [PMID: 3790399 PMCID: PMC1401178 DOI: 10.1111/j.1365-2125.1986.tb02930.x] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/07/2023] Open
Abstract
Normotensive male volunteers (n = 8) either abstained from ethanol for 4 days or consumed 66 g of ethanol per day in an open, crossed, random order study. Mean arterial pressures rose by an average of 5.4 mmHg following the ethanol phase of the study (P less than 0.001). Plasma noradrenaline (NA) concentration was higher during ethanol ingestion (P less than 0.01), principally because of a significant reduction in NA clearance of -1.51 l min-1 m-2 (P less than 0.05). In contrast, NA spillover or release rates did not significantly differ between the two study periods. Total plasma calcium levels were significantly lower (P less than 0.05) following the ethanol compared to the control period. These data do not appear to support the proposition that regular alcohol consumption raises blood pressure by producing a generalised increase in sympathetic activity.
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Abstract
The blood pressures of 252 men and 250 women, living in both urban and rural Zimbabwe, were measured on three separate occasions. Food and alcohol intakes were determined using a 3-day weighed diet survey checked by means of a detailed interview. Anthropometric data were also collected. No relationship was found between mean blood pressures and the alcohol intake for any socioeconomic group. Using only the first of the three blood pressure measurements, a correlation between systolic pressure and alcohol intake was found for white males (r = 0.234, P less than 0.05), and just missed statistical significance (r = 0.156, P = 0.065) for black middle class males. No relationship was found between blood pressure and alcohol consumption for black working class males, or for females. Epidemiological evidence suggests that alcohol consumption is associated with increased blood pressure. However, a convincing physiological mechanism is lacking. It is suggested that psychological factors may be partly responsible for this relationship.
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Wright JW, Morseth SL, Abhold RH, Harding JW. Elevations in plasma angiotensin II with prolonged ethanol treatment in rats. Pharmacol Biochem Behav 1986; 24:813-8. [PMID: 3012594 DOI: 10.1016/0091-3057(86)90416-8] [Citation(s) in RCA: 58] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/03/2023]
Abstract
Chronic alcohol consumption frequently leads to hypertension in humans. While previous reports have implicated the renin-angiotensin system as a potential mediator of this effect, plasma angiotensin II (AII) levels were either not measured or yielded negative results. The present investigation noted significant elevations in circulating AII in rats intubated daily with ethanol (4 g/kg) for 50 days. Animals administered ethanol only once evidenced AII concentrations equivalent with water intubated controls. Radioligand binding assay data indicated no differences in the number or affinity of Sar1,Ile8-AII binding sites in the thalamus, septum-anterior ventral third ventrical region or adrenal gland comparing those groups chronically treated with ethanol to water intubated controls. These results may support a role for the vasoconstrictive hormone AII in the etiology of alcohol-induced hypertension.
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Puddey IB, Beilin LJ, Vandongen R. Effect of regular alcohol use on blood pressure control in treated hypertensive subjects: a controlled study. Clin Exp Pharmacol Physiol 1986; 13:315-8. [PMID: 3731535 DOI: 10.1111/j.1440-1681.1986.tb00355.x] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/07/2023]
Abstract
Forty-four males with treated essential hypertension and a moderate-to-heavy alcohol intake participated in a randomized controlled crossover trial of the effects of varying alcohol intake on blood pressure control. Usual antihypertensive therapy was maintained unchanged throughout. Self-reported alcohol consumption fell from 452 ml ethanol/week (s.e.m. = 29) during normal drinking habits to 64 ml/week (s.e.m. = 8) while drinking low alcohol content beer. Mean systolic and diastolic blood pressures were significantly lower during the last 2 weeks of reduced alcohol (supine 5.0 mmHg, s.e.m. = 1.4, and 3.0 mmHg, s.e.m. = 0.9, respectively; erect 5.9 mmHg, s.e.m. = 1.6, and 2.9 mmHg, s.e.m. = 1.0, respectively). Body weight was also lower (0.94 kg, s.e.m. = 0.25) at the conclusion of the low alcohol intake period. Regression analysis suggested that reduction in alcohol intake contributed independently to the fall in both systolic and diastolic blood pressure, while weight change contributed independently to the fall in systolic blood pressure alone. It was concluded that curtailing moderate to heavy alcohol intake leads to improved blood pressure control in treated essential hypertensive males.
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Gitlow SE, Dziedzic LB, Dziedzic SW. Alcohol and hypertension: implications from research for clinical practice. J Subst Abuse Treat 1986; 3:121-9. [PMID: 3531537 DOI: 10.1016/0740-5472(86)90061-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/06/2023]
Abstract
Despite the fact that recent epidemiological and laboratory studies appear to confirm that alcohol has an effect upon blood pressure, its impact has largely been ignored in clinical practice. This study was undertaken in an effort to answer four basic questions Is there an association between blood pressure and ethanol ingestion and if so is it causal or related to common genetic and/or environmental factors?; If an association exists, what is its likely physiological mechanism?; What additional studies are needed in order to further elucidate the relationship between alcohol and blood pressure?; What clinical recommendations, if any, are justified with our present state of knowledge?
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Howes LG, Reid JL. Decreased vascular responsiveness to noradrenaline following regular ethanol consumption. Br J Clin Pharmacol 1985; 20:669-74. [PMID: 4091997 PMCID: PMC1400820 DOI: 10.1111/j.1365-2125.1985.tb05126.x] [Citation(s) in RCA: 30] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/08/2023] Open
Abstract
Ten normal volunteers consumed 80 g of ethanol per day or abstained from ethanol for 4 consecutive days prior to measurements of blood pressure, heart rate, vascular responsiveness to noradrenaline (NA) and angiotensin II (AII) infusions and sympathetic responsiveness to isometric handgrip exercise in an open, random order, crossed study. Supine systolic and diastolic pressures and heart rates, and erect systolic pressures rose significantly following ethanol. Vascular responsiveness to NA infusions was reduced in all subjects following ethanol, while responses to AII infusions did not show a consistent pattern of change. Plasma renin activity, plasma NA and adrenaline concentrations, and concentrations of the NA metabolite 3,4 dihydroxyphenylethylene glycol (DHPG) did not significantly differ following ethanol and control treatments. The rise in plasma NA following 2 min isometric handgrip at 50% of maximal effort was greater following ethanol (0.24 +/- 0.21 nM) than control (0.12 +/- 0.10 nM) but the difference did not reach statistical significance. The pressor effect of regular ethanol consumption and the reduced vascular reactivity to NA may both be the result of an increase in sympathetic activity that was not large enough to measurably alter resting plasma NA concentrations.
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Heidland A, Hörl WH, Schaefer RM, Teschner M, Weipert J, Heidbreder E. Role of alcohol in clinical nephrology. KLINISCHE WOCHENSCHRIFT 1985; 63:948-58. [PMID: 4057921 DOI: 10.1007/bf01738150] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
Abstract
Different nephrological derangements are observed in severe alcoholics. Until now the direct toxicity of ethanol is only shown in the fetal alcohol syndrome with various malformations of the genitourinary tract. In the adult the kidney is often involved in the development, maintenance and counterregulation of complex electrolyte disturbances like phosphate and potassium hypoglycemia etc. The alcohol associated retention of urate, induced by hyperlactatemia and/or increased beta-hydroxybutyrate concentration is only rarely complicated by urate nephropathy. Alcohol intoxication (acute and chronic) predisposes to rhabdomyolysis with the risk of acute renal failure. There are some hints that chronic alcoholism with myopathy increases the vulnerability of the kidney for further toxic agents. In rats glycerol induced renal failure is enhanced by alcohol pretreatment. Finally, regular alcohol consumption raises the blood pressure, which per se is a risk factor for renal damage.
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Abstract
The effects of acute alcohol consumption and abstinence on blood pressure were studied in normal healthy subjects and in non-drinking and regularly drinking hypertensive patients. All subjects drank alcohol (1 g/kg body weight daily) for 5 days then abstained for 5 days. There was no significant difference in blood pressure in normal subjects during and after alcohol ingestion. However, in hypertensive non-drinkers both systolic and diastolic pressures when standing were significantly higher during the period of alcohol intake; supine blood pressure was not significantly higher. In hypertensive patients who drank regularly, standing and supine systolic and diastolic blood pressures were significantly higher during the period of drinking.
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