⚡ Aldosterone is a mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex. It regulates sodium (Na⁺) and potassium (K⁺) balance, blood pressure 🩸, and fluid homeostasis 💧. Although its main actions are renal, it also affects the heart and blood vessels.

🧬 Synthesis & Regulation

Synthesis: Derived from cholesterol via key enzymes (cholesterol desmolase, 21-hydroxylase, aldosterone synthase).
Regulators:
- 🌀 RAAS: Angiotensin II → powerful stimulus for aldosterone secretion.
- 🟤 Plasma potassium: ↑ K⁺ → ↑ aldosterone release.
- 🧠 ACTH: Minor effect (mainly regulates cortisol, but stimulates aldosterone transiently).
- 🧂 Sodium: Low Na⁺ indirectly activates RAAS → aldosterone release.

⚙️ Mechanism of Action

Aldosterone diffuses into target cells → binds to mineralocorticoid receptors.
The complex moves to the nucleus → activates transcription of genes coding for Na⁺ and K⁺ transport proteins (e.g. ENaC channels, Na⁺/K⁺-ATPase).
Result → Na⁺ reabsorption (water follows), K⁺ and H⁺ excretion.

💡 Effects

Kidneys:
- ↑ Na⁺ reabsorption → ↑ water retention → ↑ BP.
- ↑ K⁺ excretion → prevents hyperkalaemia.
- ↑ H⁺ secretion → links to metabolic alkalosis.
Cardiovascular system: Can promote fibrosis and vascular remodelling (important in HF and hypertension).
Other tissues: Intestines, sweat glands, salivary glands → conserve Na⁺, excrete K⁺.

⚠️ Clinical Relevance

Hyperaldosteronism (Conn’s syndrome, adrenal hyperplasia):
- HTN + hypokalaemia + metabolic alkalosis.
- Secondary causes: heart failure, cirrhosis, nephrotic syndrome (due to excess RAAS activation).
Hypoaldosteronism:
- Leads to hyperkalaemia + hyponatraemia + hypotension.
- Seen in Addison’s disease, or resistance states (pseudohypoaldosteronism).
Aldosterone antagonists: 🩺 Spironolactone, Eplerenone → block MR receptor, reduce fibrosis, used in HTN, HF, Conn’s.

📚 Exam Tips

Conn’s triad: HTN + hypokalaemia + alkalosis.
Spironolactone side effects: gynaecomastia, hyperkalaemia.
Clue in OSCE: Resistant hypertension with low renin + high aldosterone → think Conn’s.

📝 Summary

Aldosterone maintains Na⁺, K⁺, BP, and acid-base balance. Its secretion is controlled by RAAS, K⁺ levels, ACTH, and Na⁺ status. Excess causes hypertension + hypokalaemia; deficiency causes hypotension + hyperkalaemia. Therapeutically, aldosterone antagonists are vital in managing heart failure and resistant hypertension.

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Aldosterone Physiology