Cardiac markers: Role in the pathogenesis of arterial hypertension

Table 3 Role of matrix metalloproteinases, tissue inhibitors of metalloproteinases, N-terminal pro-B-type natriuretic peptide, plasma renin activity levels, and dynorphin in the pathogenesis of arterial hypertension

Ref.	Cardiac markers	The main finding of cardiac markers in arterial hypertension
Prado et al[52], 2021	Matrix metalloproteinase activity	Imbalanced vascular matrix metalloproteinase activity promotes vascular dysfunction and a variety of structural alterations, resulting in vascular remodeling in hypertension
Flamant et al[53], 2007	Matrix metalloproteinase-9 activity	The onset of angiotensin II-induced hypertension is accompanied by increased matrix metalloproteinase-9 activity in conductance vessels; absence of matrix metalloproteinase-9 activity results in vessel stiffness and increased pulse pressure; and matrix metalloproteinase-9 activation is associated with a beneficial role early on in hypertension by preserving vessel compliance and alleviating blood pressure increase
Hopps et al[54], 2017	Matrix metalloproteinases and tissue inhibitors of metalloproteinases	The authors believe that in clinical practice a strategic antihypertensive therapy directed to the matrix metalloproteinase profile may be useful to decrease the risk of cardiovascular complications
Valente et al[55], 2020	Matrix metalloproteinase-9 concentrations	Matrix metalloproteinase-9 concentrations are significantly higher in the hypertensive crisis groups (urgency and emergency) compared to the control groups. Therefore, matrix metalloproteinase-9 may be a biomarker or mediator of pathophysiologic pathways in cases of acute elevations of blood pressure
Kuliczkowski et al[56], 2019	Tissue inhibitors of metalloproteinases-4, matrix metalloproteinase-2	Data showed that patients with coronary artery disease presented higher tissue inhibitors of metalloproteinase-4 and lower matrix metalloproteinase-2 concentrations regardless of hypertension and diabetes mellitus.
Tayebjee et al[57], 2004	Matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1	Increased circulating matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1 at baseline in patients with hypertension could reflect an increased deposition and retention of type I collagen at the expense of other components of extracellular matrix within the cardiac and vascular extracellular matrix
Robert et al[58], 1997	Matrix metalloproteinases	Observations suggest that depression of the degradative pathway is partly responsible for age-associated fibrosis. Thus, matrix metalloproteinase has differing involvements in the cardiac remodeling associated with hypertension or aging
Marchesi et al[61], 2012	Matrix metalloproteinase-2, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1	Suggested that matrix metalloproteinase-2, matrix metalloproteinas-9 as well as tissue inhibitor of metalloproteinases-1 could have a role as biomarkers of cardiovascular remodeling in hypertension patients
Nakatsu et al[64], 2007	Plasma B-type natriuretic peptide	Hypertensive patients with abnormal diurnal blood pressure variation patterns (non-dippers, extreme dippers, and risers) showed higher plasma B-type natriuretic peptide levels than those with normal circadian blood pressure variation (dippers)
Seven et al[65], 2015	N-terminal pro-B-type natriuretic peptide	Elevated serum concentrations of N-terminal pro-B-type natriuretic peptide are associated with prevalent hypertension whereas lower concentrations associate with incident hypertension
Freitag et al[66], 2003	Plasma brain natriuretic peptide	Higher plasma brain natriuretic peptide levels were associated with an increased risk of blood pressure progression in men but not women
Brunner et al[69], 1972	High plasma renin activity	Essential hypertension would appear to show that individuals with low plasma renin activity had a significantly lower incidence of myocardial infarction and stroke over about 10 years of observation compared to individuals with normal or high plasma renin activity
Sever et al[70], 2012	Plasma renin activity levels	Elevated plasma renin activity levels in a hypertensive population with no pre-existing cardiovascular disease do not indicate the future occurrence of cardiovascular events
Haber et al[71], 1979	Renin	Renin is crucial for regulating blood pressure in the salt- or volume-depleted condition and is in charge of the early stages of renovascular hypertension
Laragh et al[74], 2011	Plasma renin activity	Plasma renin activity testing can be used to guide the commencement, addition, or subtraction of anti-sodium-volume dependent or anti-renin-angiotensin antihypertensive drug types in hypertensive patients
Fontana et al[78], 1993	Dynorphin	Dynorphin modulates sympathetic activity via stimulation of atrial natriuretic factor which can reduce BP in hypertensive subjects
McConnaughey et al[79], 1992	Dynorphin	Findings imply that alterations in the opioid system's hippocampus receptors may be important for the main blood pressure-control mechanism
Wang et al[80], 1994	Dynorphin-A (1-8)	Dynorphin-A (1-8) injected into the hippocampal formation causes a significant drop in blood pressure in conscious hypertensive and normotensive rats, but not heart rate