Angiotensin II
Also known as: Ang II, angiotensin, renin–angiotensin–aldosterone system, RAAS
An octapeptide formed from angiotensin I by angiotensin-converting enzyme that raises blood pressure and conserves salt and water by vasoconstriction, aldosterone and ADH release, thirst and direct renal sodium retention.
Overview
Angiotensin I (inactive decapeptide) is converted to angiotensin II mainly by angiotensin-converting enzyme (ACE) on the endothelium of the pulmonary capillaries (and in the kidney). ACE is identical to kininase II, so it also degrades vasodilator bradykinin — explaining the cough and angioedema caused by ACE inhibitors.
Angiotensin II acts on AT1 receptors (Gq): (1) arteriolar vasoconstriction, raising total peripheral resistance; in the kidney it constricts the efferent more than the afferent arteriole, preserving GFR when perfusion falls; (2) stimulates aldosterone from the zona glomerulosa; (3) stimulates ADH release and thirst via the subfornical organ; (4) increases Na⁺ reabsorption in the proximal tubule (Na⁺/H⁺ exchanger NHE3); (5) enhances sympathetic transmission; (6) chronically promotes cardiac and vascular hypertrophy and fibrosis. AT2 receptors mediate partly opposing (vasodilator, antiproliferative) effects. It is rapidly degraded by angiotensinases (half-life ≈1–2 min); ACE2 converts it to vasodilator angiotensin 1–7.
- Location
Formed in plasma, mainly in the lung by endothelial ACE, from renal renin acting on hepatic angiotensinogen. Targets: arterioles, adrenal cortex, hypothalamus, kidney, heart.
Function
- Vasoconstriction and increased blood pressure.
- Stimulation of aldosterone, ADH and thirst.
- Proximal tubular Na⁺ reabsorption and preservation of GFR (efferent constriction).
- Physiology
Class: octapeptide. Receptor: AT1 (Gq/IP₃) — main actions; AT2. Half-life ≈1–2 min.
- Regulation
Formation is governed by renin secretion (rate-limiting); inhibits renin by short-loop feedback.
Clinical significance
RAAS blockade
ACE inhibitors (ramipril) and angiotensin receptor blockers (losartan) treat hypertension, heart failure and proteinuric kidney disease. Adverse effects: hyperkalaemia, a rise in creatinine (loss of efferent tone), cough and angioedema (ACE inhibitors). Both are contraindicated in pregnancy (fetal renal dysgenesis).
Test yourself
Which zone of the adrenal cortex is primarily controlled by angiotensin II and serum potassium rather than ACTH?
- Zona glomerulosa
- Zona fasciculata
- Zona reticularis
- Adrenal medulla
Answer: Zona glomerulosa
Zona glomerulosa cells express aldosterone synthase (CYP11B2) and respond mainly to angiotensin II (AT1, Gq) and hyperkalaemia (depolarisation). ACTH has only a minor, transient effect, which is why pituitary failure spares aldosterone.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.