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[Biochemistry](https://durgical.com/en/biochemistry/) · Molecule

# Aldosterone

The zona glomerulosa mineralocorticoid: it makes the kidney keep sodium and water and excrete potassium and hydrogen ions.

Updated 2026-11-01

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## Key facts

- Angiotensin II and high potassium stimulate it; ACTH plays a minor role.
- It acts on the mineralocorticoid receptor of collecting duct principal cells: more ENaC channels and more Na⁺/K⁺ pump.
- Result: sodium and water retention, potassium and hydrogen ion loss (metabolic alkalosis).
- Its precursor 11-deoxycorticosterone also has mineralocorticoid action: that is why some adrenal hyperplasias come with hypertension.

**Formula**
C21H28O5

**PubChem**
[CID 5839](https://pubchem.ncbi.nlm.nih.gov/compound/5839)

## Structure

- A 21-carbon steroid with an aldehyde on carbon 18 (hence its name), which forms a hemiacetal with the 11β-hydroxyl.
- Its last step is done by aldosterone synthase (CYP11B2): 11β-hydroxylation, 18-hydroxylation and 18-oxidation.

## Clinical notes

- Primary hyperaldosteronism (Conn syndrome): hypertension, low potassium and suppressed renin.
- Spironolactone and eplerenone block its receptor (resistant hypertension, heart failure, cirrhosis with ascites).
- Its lack in salt-wasting adrenal hyperplasia causes low sodium, high potassium and dehydration in the newborn.

## Related conditions

- [Arterial hypertension](https://durgical.com/en/conditions/arterial-hypertension/)
- [Adrenal insufficiency](https://durgical.com/en/conditions/adrenal-insufficiency/)
- [Congenital adrenal hyperplasia due to 21-hydroxylase deficiency](https://durgical.com/en/conditions/congenital-adrenal-hyperplasia-due-to-21-hydroxylase-deficiency/)
- [Heart failure](https://durgical.com/en/conditions/heart-failure/)

## Related

- [Adrenal enzymes and congenital adrenal hyperplasia](https://durgical.com/en/biochemistry/topics/adrenal-enzymes-and-congenital-adrenal-hyperplasia/)
- [21-Hydroxylase (CYP21A2)](https://durgical.com/en/biochemistry/enzymes/21-hydroxylase/)
- [11β-Hydroxylase (CYP11B1)](https://durgical.com/en/biochemistry/enzymes/11-hydroxylase/)
- [Cortisol](https://durgical.com/en/biochemistry/molecules/cortisol/)
- [Na⁺/K⁺-ATPase (sodium pump)](https://durgical.com/en/biochemistry/enzymes/na-k-atpase/)
- [Nuclear receptors](https://durgical.com/en/biochemistry/topics/nuclear-receptors/)
- [Angiotensin-converting enzyme (ACE)](https://durgical.com/en/biochemistry/enzymes/angiotensin-converting-enzyme/)

## Test yourself

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

## Which two main stimuli raise aldosterone?

Angiotensin II and hyperkalaemia.

## Which cells does aldosterone act on, and which proteins does it increase?

Collecting duct principal cells; it increases ENaC sodium channels and the Na⁺/K⁺-ATPase.

## Which lab changes does primary hyperaldosteronism cause?

Hypokalaemia, metabolic alkalosis and suppressed renin with high aldosterone.

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Molecules are shown in their neutral form, as the databases deposit them; in the cell the acids and phosphates are ionised.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: [Aldosterone (CID 5839)](https://pubchem.ncbi.nlm.nih.gov/compound/5839) (PubChem, NCBI, 2026) · Public domain; [NR3C2: Mineralocorticoid receptor (human)](https://www.uniprot.org/uniprotkb/P08235/entry) (UniProt, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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