In pathological contexts—such as chronic stress or hypertension—SNS overactivation and PNS suppression skew this equilibrium, elevating catecholamine levels and triggering tachycardia, arrhythmias, or heart failure (HF).117,122–124 Excessive SNS drive also stimulates juxtaglomerular cells to release renin, activating the renin–angiotensin system (RAS), which induces vasoconstriction, promotes myocyte hypertrophy, and fosters inflammation, exacerbating atherosclerotic cardiovascular disease (ASCVD) and HF progression.125–127. Here, REN is linked to hydrops fetalis.