Renin-angiotensin-aldosterone system (RAAS) (RAAS)

The Renin-angiotensin-aldosterone system (RAAS) is a fundamental hormonal signaling cascade that regulates systemic blood pressure, fluid volume, and electrolyte balance [10, 15]. The pathway begins with the secretion of the enzyme renin from the kidneys, which converts liver-derived angiotensinogen into angiotensin I; this is subsequently processed by angiotensin-converting enzyme (ACE) into the primary effector peptide, angiotensin II [1, 13]. Angiotensin II exerts potent vasoconstrictive, pro-inflammatory, and pro-fibrotic effects primarily through the G protein-coupled AT1 receptor, while also stimulating the adrenal cortex to release aldosterone, which promotes renal sodium and water retention [3, 10, 16]. Dysregulation or chronic overactivation of the RAAS is a central driver of hypertension, heart failure, and chronic kidney disease, contributing to pathological cardiovascular remodeling and progressive renal damage [6, 14]. Consequently, the RAAS is one of the most extensively targeted systems in clinical medicine, with drug classes such as ACE inhibitors, angiotensin receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) serving as standard-of-care treatments [1, 15]. Modern research also highlights the counter-regulatory ACE2/Ang-(1-7)/Mas receptor axis, which opposes the classical pathway's harmful effects and represents a promising area for novel therapeutic development [11, 12].

Other names

Renin-angiotensin systemRASRAAS cascadeAngiotensin signaling pathway

Inhibition of angiotensin-converting enzyme (ACE), blockade of angiotensin II type 1 (AT1) receptors, direct inhibition of renin activity, antagonism of mineralocorticoid receptors, and enhancement of the protective ACE2/Ang-(1-7)/Mas receptor axis.