The renin-angiotensin-aldosterone system
One pathway, four drug classes: where ACE inhibitors, ARBs, aldosterone antagonists, and renin inhibitors each cut in.
Click any node for its role, or open a question below to light the causal path.
Read this pathway as text
Falling renal perfusion triggers renin release from the juxtaglomerular apparatus. Renin converts angiotensinogen (from the liver) to angiotensin I. Angiotensin-converting enzyme (ACE), abundant in lung endothelium, converts angiotensin I to angiotensin II. Angiotensin II acts on AT1 receptors to vasoconstrict, stimulate aldosterone release from the adrenal cortex, and preferentially constrict the efferent arteriole of the glomerulus. Aldosterone promotes distal sodium and water retention. ACE also degrades bradykinin; inhibiting ACE therefore raises bradykinin, which causes the characteristic dry cough and contributes to angioedema. ACE inhibitors block the angiotensin I to II conversion; ARBs block AT1 receptors directly and leave bradykinin alone, which is why they rarely cough.
Last reviewed 2026-08-15 · Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.