Sympathetic nervous system activation and heart failure: Current state of evidence and the pathophysiology in the light of novel biomarkers

Figure 1 A diagram showing basic etiology, pathophysiology and compensatory mechanisms that are activated in heart failure. CO: Cardiac output; COPD: Chronic obstructive pulmonary disease; HF: Heart failure; HFmrEF: Heart failure with midrange ejection fraction; HFpEF: Heart failure with preserved ejection fraction; HFrEF: Heart failure with reduced ejection fraction; MAP: Mean arterial pressure; RAAS: Renin-angiotensin-aldosterone system; SV: Stroke volume.

Figure 2 The function and physiological actions of beta-adrenergic receptors and adrenergic signaling. β: Beta; G_i: Inhibitory alpha subunit of G protein; G_s: Stimulatory alpha subunit of G protein; NO: Nitric oxide.

Figure 3 Physiological and pathophysiological implications of neuropeptide Y and galanin with respect to cardiovascular system. Ach: Acetylcholine; ERP: Effective refractory period; HF: Heart failure; IRI: Ischemia-reperfusion injury; LV: Left ventricular; MI: Myocardial infarction; NPY: Neuropeptide Y; STEMI: ST-elevation myocardial infarction; VIP: Vasoactive intestinal peptide.

Figure 4 Physiological and pathophysiological implications of endothelin-1 in circulation and on various cell types and adrenergic neurons. ECE: Endothelin converting ezyme; ET-1: Endothelin-1; NE: Norepinephrine; NO: Nitric oxide; PGI₂: Prostacyclin (prostaglandin I2); VSMCs: Vascular smooth muscle cells.

Figure 5 Mechanism of catestatin autocrine modulation of chromaffin cell in the adrenal medulla during sympathetic stimulation. ACh: Acetylcholine; ATP: Adenosine triphosphate; Ca²⁺: Calcium; ChgA: Chromogranin A; nAchR: Neuronal type of nicotinic cholinergic receptors; Na⁺: Sodium; NPY: Neuropeptide Y.