Renin-angiotensin system (RAS) (RAS)

The Renin-angiotensin system (RAS) is a complex hormonal signaling pathway essential for the regulation of systemic blood pressure, fluid volume, and electrolyte homeostasis [StatPearls, NBK470410]. It functions through a proteolytic cascade where the enzyme renin cleaves angiotensinogen to produce angiotensin I, which is then converted to the active octapeptide angiotensin II by angiotensin-converting enzyme (ACE) [NIH, PMC4132734]. Angiotensin II acts primarily on the Angiotensin II type 1 (AT1) receptor to induce potent vasoconstriction, stimulate aldosterone release, and promote renal sodium retention [PubMed, 24078457]. Overactivation of this system is a primary contributor to the development of essential hypertension, congestive heart failure, and progressive renal damage [StatPearls, NBK470410]. Pharmacological intervention in the RAS is a cornerstone of modern cardiovascular therapy, utilizing ACE inhibitors, angiotensin receptor blockers (ARBs), and direct renin inhibitors to lower blood pressure and provide organ protection [PubMed, 15102974]. These therapies are particularly effective in reducing the risk of stroke, myocardial infarction, and the progression of diabetic nephropathy [NIH, PMC4132734]. Beyond its systemic hemodynamic roles, the RAS also influences local tissue processes including inflammation, oxidative stress, and fibrotic remodeling in the heart and kidneys [PubMed, 24078457]. Understanding the balance between the classical ACE/Angiotensin II/AT1R axis and the counter-regulatory ACE2/Angiotensin-(1-7)/Mas receptor axis is an area of active research for novel therapeutics [Wikipedia, Renin-angiotensin system].

Other names

Renin-angiotensin-aldosterone systemRAASRenin-angiotensin system signaling pathway

Inhibition of angiotensin-converting enzyme, blockade of angiotensin II type 1 receptors, direct renin inhibition, and mineralocorticoid receptor antagonism [StatPearls, NBK470410].