Aldosterone
Also known as: mineralocorticoid
The main mineralocorticoid, made by the zona glomerulosa in response to angiotensin II and high potassium, that promotes Na⁺ reabsorption and K⁺ and H⁺ secretion in the distal nephron, regulating extracellular volume, blood pressure and potassium.
Overview
Aldosterone is the final product of the renin–angiotensin–aldosterone system. It enters principal cells of the late distal convoluted tubule, connecting tubule and cortical collecting duct and binds the mineralocorticoid receptor (MR). Gene induction (including SGK1) increases the number and activity of apical epithelial Na⁺ channels (ENaC), basolateral Na⁺/K⁺-ATPase and apical ROMK K⁺ channels. Sodium reabsorption makes the lumen more negative, which drives K⁺ secretion through ROMK and H⁺ secretion by the H⁺-ATPase of α-intercalated cells. Water follows sodium (if ADH is present), expanding extracellular volume.
Aldosterone acts similarly on the distal colon, sweat and salivary glands. Non-genomic effects and MR activation in heart and vessels promote fibrosis and remodelling — the rationale for MR antagonists in heart failure. With sustained aldosterone excess, sodium retention plateaus after a few days (aldosterone escape, via pressure natriuresis and ANP), so oedema is absent while potassium loss continues.
- Location
Source: zona glomerulosa of the adrenal cortex. Targets: principal and α-intercalated cells of the distal nephron; colon; sweat and salivary glands; heart and vessels.
Function
- Increases renal Na⁺ reabsorption (and so extracellular volume and blood pressure).
- Increases K⁺ secretion — the main hormonal defence against hyperkalaemia.
- Increases H⁺ secretion (acid excretion).
- Physiology
Class: steroid (C21 mineralocorticoid). Receptor: mineralocorticoid receptor (nuclear, NR3C2). Half-life ≈15–20 min (weakly protein-bound). Secretion ≈100–150 µg/day.
- Regulation
Stimulated by angiotensin II (AT1 — Gq), raised plasma K⁺ (direct depolarisation of glomerulosa cells; very sensitive) and, minimally, ACTH. Inhibited by ANP, hypokalaemia, heparin and dopamine. Low sodium intake increases it via the renin–angiotensin system.
Clinical significance
Primary hyperaldosteronism
Hypertension, hypokalaemia (in a minority), metabolic alkalosis and suppressed renin; caused by bilateral hyperplasia or an aldosterone-producing adenoma (Conn syndrome).
Hypoaldosteronism
Addison disease, hyporeninaemic hypoaldosteronism (diabetic nephropathy), ACE inhibitors/ARBs, heparin: hyperkalaemia with mild hyperchloraemic metabolic acidosis (type 4 renal tubular acidosis).
Drugs
Spironolactone and eplerenone (MR antagonists) and amiloride (ENaC blocker) are potassium-sparing diuretics used in hyperaldosteronism, heart failure, resistant hypertension and ascites; fludrocortisone replaces mineralocorticoid in Addison disease.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.