Renin–angiotensin–aldosterone system (RAAS)

The renin–angiotensin–aldosterone system (RAAS) is a complex hormonal signaling cascade regulating blood pressure, fluid balance, and vascular tone. Key molecular targets within the RAAS include enzymes (renin, angiotensin-converting enzyme/ACE), peptide hormones (angiotensin II, aldosterone), and their receptors (AT1, AT2, mineralocorticoid receptor). Overactivation of the RAAS contributes to hypertension, cardiovascular, and kidney diseases through mechanisms including vasoconstriction, sodium retention, inflammation, cell proliferation, fibrosis, and tissue remodeling. Pharmacological inhibition of RAAS—via ACE inhibitors, ARBs, renin inhibitors, or mineralocorticoid antagonists—provides well-established protection for the heart, blood vessels, and kidneys, and is a mainstay of therapy for multiple cardiovascular and renal conditions; however, long-term therapy requires monitoring for dose-limiting adverse effects and resistance phenomena.

Other names

Renin–angiotensin systemRASRenin–angiotensin–aldosterone axis

Inhibition of angiotensin II production (by blocking ACE or renin); Antagonism of angiotensin II receptors (primarily AT1 receptor); Antagonism of aldosterone receptor; Combination inhibition (e.g., neprilysin and ARB).