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[Physiology](https://durgical.com/en/physiology/) · [Endocrine](https://durgical.com/en/physiology/#s-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](https://durgical.com/en/anatomy/suprarenal-gland/) · [Right adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland-abdomen/) · [Kidneys](https://durgical.com/en/anatomy/kidney/)

## Key points

- Two strong stimuli: angiotensin II and high plasma potassium (direct effect). ACTH adds little and only briefly.
- Excess: hypertension, hypokalemia and metabolic alkalosis. Deficit: hyperkalemia, mild metabolic acidosis and salt wasting.
- Primary hyperaldosteronism (Conn): high aldosterone with suppressed renin; high aldosterone/renin ratio.
- Aldosterone "escape": primary excess causes no edema because high pressure and natriuretic peptide return the sodium.
- ACE inhibitors and ARBs lower aldosterone and can raise potassium.

## 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

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

### Hormone axes and feedback

Renin–angiotensin–aldosterone system **Lesion** 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

**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

| Situation | Renin | Aldosterone | Potassium and pressure |
| --- | --- | --- | --- |
| [Primary hyperaldosteronism (Conn)](https://durgical.com/en/conditions/arterial-hypertension/) | ↓ | ↑ | K⁺ ↓, hypertension |
| [Secondary hyperaldosteronism (renal stenosis, heart failure, cirrhosis)](https://durgical.com/en/conditions/heart-failure/) | ↑ | ↑ | K⁺ ↓ or normal; variable pressure |
| [Primary adrenal insufficiency](https://durgical.com/en/conditions/adrenal-insufficiency/) | ↑ | ↓ | K⁺ ↑, hypotension |
| [Hyporeninemic hypoaldosteronism (diabetes, nephropathy)](https://durgical.com/en/conditions/hyperkalaemia/) | ↓ | ↓ | K⁺ ↑, type 4 renal tubular acidosis |
| [Apparent mineralocorticoid excess (licorice)](https://durgical.com/en/conditions/hypokalaemia/) | ↓ | ↓ | 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.

## Memory aid

Aldosterone swaps sodium for potassium at the collecting-duct counter: one comes in, the other goes out.

## 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.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/aldosterone-actions-and-control/)

## See it in 3D

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

- [Left adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland/)
- [Right adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland-abdomen/)
- [Kidneys](https://durgical.com/en/anatomy/kidney/)

## Related topics

- [The renin–angiotensin–aldosterone system](https://durgical.com/en/physiology/the-renin-angiotensin-aldosterone-system/)
- [Potassium balance](https://durgical.com/en/physiology/potassium-balance/)
- [Distal tubule and collecting duct](https://durgical.com/en/physiology/distal-tubule-and-collecting-duct/)
- [Sodium and extracellular volume regulation (with natriuretic peptides)](https://durgical.com/en/physiology/sodium-and-extracellular-volume-regulation/)
- [Metabolic alkalosis and its compensation](https://durgical.com/en/physiology/metabolic-alkalosis-and-its-compensation/)
- [The adrenal cortex: zones, hormones and androgens](https://durgical.com/en/physiology/the-adrenal-cortex-zones-hormones-and-androgens/)
- [The HPA axis and its circadian rhythm](https://durgical.com/en/physiology/the-hpa-axis-and-its-circadian-rhythm/)

## Related conditions

- [Hyperkalaemia](https://durgical.com/en/conditions/hyperkalaemia/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)
- [Adrenal insufficiency](https://durgical.com/en/conditions/adrenal-insufficiency/)
- [Arterial hypertension](https://durgical.com/en/conditions/arterial-hypertension/)

## In Biochemistry

- [Aldosterone](https://durgical.com/en/biochemistry/molecules/aldosterone/)

## In Pharmacology

- [ACE inhibitors](https://durgical.com/en/pharmacology/classes/ace-inhibitors/)
- [Angiotensin II receptor blockers (ARBs)](https://durgical.com/en/pharmacology/classes/angiotensin-ii-receptor-blockers/)

[← All of physiology](https://durgical.com/en/physiology/)

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](https://openstax.org/books/anatomy-and-physiology-2e/pages/17-6-the-adrenal-glands) (OpenStax (Rice University), 2022); [Aldosterone Test: MedlinePlus Medical Test](https://medlineplus.gov/lab-tests/aldosterone-test/) (MedlinePlus, US National Library of Medicine, 2024); [High potassium level: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/001179.htm) (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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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/aldosterone-actions-and-control/