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Physiology · Endocrine

Aldosterone: actions and control !

  • Regulation
  • Exam priority: high

Aldosterone makes the kidney keep sodium and excrete potassium and hydrogen. Angiotensin II and high potassium trigger it.

Updated 2026-11-01

Also called: Mineralocorticoids, Hyperaldosteronism

See it in 3D: Left adrenal gland · Right adrenal gland · Kidneys

What it is

Aldosterone comes from the zona glomerulosa and acts on the principal cells of the collecting duct and late distal tubule. Through its nuclear receptor it increases ENaC channels, Na⁺/K⁺-ATPase and potassium channels: sodium enters, potassium leaves, and in intercalated cells hydrogen leaves. It is the key potassium hormone and one of the two big volume hormones.

How it works, step by step

  1. Aldosterone enters the principal cell and binds the mineralocorticoid receptor, shielded from cortisol by 11β-HSD2.
  2. The complex switches on genes such as SGK1, which stops ENaC breakdown: more channels sit in the luminal membrane.
  3. More sodium enters from the lumen; basolateral Na⁺/K⁺-ATPase pumps it to blood and brings potassium into the cell.
  4. The lumen becomes more negative and potassium leaves through ROMK into the urine.
  5. In α-intercalated cells it stimulates H⁺-ATPase: acid is secreted and new bicarbonate is made.

Hormone axes and feedback

Hormone axes and feedback: Renin–angiotensin–aldosterone system ↓ renal perfusion · ↓ NaCl at the macula densa · sympathetic β₁−−++++++Kidney (juxtaglomerular cells)ReninLiver: angiotensinogen →Ang ILung (endothelial ACE) →Ang IIAdrenal (glomerulosa)AldosteroneAng II alsoVasoconstr. · ADH · thirstResult↑ BP and volume

Renin–angiotensin–aldosterone systemLesion None (normal)

Tap a box to see the hormone, or choose a lesion to see the lab pattern.

  • Stimulates (+)
  • Inhibits / negative feedback (−)
  • Level ↑
  • Level ↓
Illustrative schematic drawn by Durgical: simplified axes and classic lab patterns; not for clinical decisions.

The nephron: segments, transporters and diuretics

The nephron: segments, transporters and diuretics CortexOuter medullaInner medulla3006009001200mOsm/kgUrineGlomerulusProximal tubuleDistal tubuleThin descendingThin ascendingThick ascendingCollecting ductJuxtaglomerularapparatusNHE3 · SGLT2Filters ≈ 180 L/dayAQP1Passive NaClNKCC2 · ROMKParacellular Ca²⁺, Mg²⁺NCC · Ca²⁺ (PTH)ENaC · ROMK/BKAQP2 (ADH)α: H⁺-ATPase · β: pendrin

Na⁺ reabsorbed ≈ 2–5%Water reabsorbed variable (ADH)

Collecting tubule and duct

  • What it does: Fine tuning: reabsorbs ≈ 2–5% of Na⁺, secretes K⁺ and H⁺ and reabsorbs water as ADH allows (urine from ≈ 50 to ≈ 1200 mOsm/kg). Principal cells handle Na⁺, K⁺ and water; intercalated cells handle acid–base.
  • Transporters: Principal: ENaC, ROMK and BK (K⁺ secretion; BK is flow-driven), apical AQP2 (ADH) and basolateral AQP3/4. α-intercalated: H⁺-ATPase and H⁺/K⁺-ATPase (secrete acid). β-intercalated: pendrin (secrete HCO₃⁻). Inner medulla: urea transporters (ADH).
  • Hormones: Aldosterone (more ENaC, ROMK, Na⁺/K⁺-ATPase and H⁺-ATPase); ADH via the V2 receptor → cAMP → AQP2 insertion; atrial natriuretic peptide curbs Na⁺ reabsorption.
  • Drugs: ENaC blockers (6) and mineralocorticoid receptor antagonists (7): K⁺-sparing (risk of hyperkalemia). V2 receptor antagonists (8, vaptans): aquaretics.
  • Disorders: Liddle syndrome (overactive ENaC: hypertension, hypokalemia, low renin and aldosterone); nephrogenic diabetes insipidus (V2 or AQP2, lithium); type 1 distal renal tubular acidosis (H⁺ secretion fails: urine pH > 5.5, hypokalemia, stones) and type 4 (hypoaldosteronism: hyperkalemia); SIADH (excess ADH).
  • Glomerulus and arterioles
  • Proximal tubule
  • Thin descending limb
  • Thin ascending limb
  • Thick ascending limb
  • Distal convoluted tubule
  • Collecting tubule and duct
  • Juxtaglomerular apparatus (macula densa)
  • Cortex
  • Medulla
  • Interstitial osmolality (≈ 300 → 1200 mOsm/kg)
Illustrative schematic drawn by Durgical (a long-loop juxtamedullary nephron); proportions and percentages are approximate and not for clinical decisions.

Regulation

  • +Angiotensin II (AT1 receptor): Main stimulus when volume or blood pressure falls.
  • +High plasma potassium: Depolarizes the glomerulosa cell and raises secretion directly.
  • +ACTH: Small, transient rise; not needed for basal secretion.
  • −Atrial natriuretic peptide: Inhibits the glomerulosa and renin when volume is in excess.
  • −Low potassium and sodium excess: Reduce secretion.

Renin and aldosterone patterns

SituationReninAldosteronePotassium and pressure
Primary hyperaldosteronism (Conn)↓↑K⁺ ↓, hypertension
Secondary hyperaldosteronism (renal stenosis, heart failure, cirrhosis)↑↑K⁺ ↓ or normal; variable pressure
Primary adrenal insufficiency↑↓K⁺ ↑, hypotension
Hyporeninemic hypoaldosteronism (diabetes, nephropathy)↓↓K⁺ ↑, type 4 renal tubular acidosis
Apparent mineralocorticoid excess (licorice)↓↓K⁺ ↓, hypertension

Clinical notes

  • Hypertension with spontaneous hypokalemia suggests primary hyperaldosteronism, a cause of secondary hypertension more common than once thought.
  • Primary adrenal insufficiency with hyperkalemia can cause arrhythmias: it is an emergency.
  • Loop and thiazide diuretics deliver more sodium to the collecting duct; with high aldosterone, potassium loss increases.

Test yourself

Think of the answer, then tap the question to see it.

Why does primary hyperaldosteronism cause metabolic alkalosis?

Aldosterone stimulates intercalated-cell H⁺-ATPase and makes the lumen more negative: more acid is secreted and new bicarbonate enters the blood; hypokalemia makes it worse.

Why is there no edema in primary hyperaldosteronism even though sodium is retained?

Escape: volume expansion raises renal perfusion pressure and natriuretic peptide, and the proximal tubule and other segments excrete the extra sodium.

Why does high potassium stimulate aldosterone without going through renin?

It directly depolarizes the glomerulosa cell, opens calcium channels and boosts synthesis; it is potassium's own control loop.

Why can an ACE inhibitor raise plasma potassium?

Lower angiotensin II means lower aldosterone; potassium secretion in the collecting duct falls and potassium builds up, especially with kidney disease.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 17.6 The Adrenal Glands (OpenStax (Rice University), 2022); Aldosterone Test: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2024); High potassium level: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 78). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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