Renin–angiotensin–aldosterone system (RAAS) (RAAS)

The Renin-angiotensin-aldosterone system (RAAS) is a multi-organ endocrine cascade that serves as a primary regulator of blood pressure, fluid volume, and electrolyte balance (StatPearls, 2023). The process begins when the kidneys release the enzyme renin in response to low blood pressure or reduced sodium levels, which then converts angiotensinogen into angiotensin I (NCBI, 2022). Angiotensin-converting enzyme (ACE) subsequently converts angiotensin I into angiotensin II, a powerful vasoconstrictor that also stimulates the adrenal cortex to release aldosterone (Ames et al., 2019). Aldosterone acts on the kidneys to promote sodium and water retention, thereby increasing blood volume and pressure (StatPearls, 2023). Chronic overactivation of this system is a major contributor to the pathogenesis of hypertension, heart failure, and chronic kidney disease (Nature Reviews Cardiology, 2020). Consequently, the RAAS is a major therapeutic focus, with drugs such as ACE inhibitors, angiotensin receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) being standard treatments to reduce cardiovascular morbidity and slow renal decline (Circulation, 2018).

Other names

Renin-angiotensin systemRASRAAS pathwayRenin-angiotensin-aldosterone axis

Drugs targeting the RAAS act by inhibiting renin activity, preventing the conversion of angiotensin I to angiotensin II via ACE inhibition, blocking the binding of angiotensin II to AT1 receptors, or antagonizing the mineralocorticoid receptor to prevent aldosterone-mediated sodium retention (StatPearls, 2023; Circulation, 2018).