Patients with primary hyperaldosteronism characteristically develop hypertension and hypokalemia but rarely develop significant peripheral edema. Which mechanism accounts for this 'aldosterone escape'?

• A Atrial natriuretic peptide release in response to expanded extracellular volume ✓
• B Downregulation of epithelial sodium channels in the collecting duct
• C Suppression of renin with secondary loss of angiotensin II vasoconstriction
• D Competitive inhibition of aldosterone receptors by cortisol

Explanation

Mineralocorticoid-driven sodium retention expands extracellular fluid volume, stretching atrial myocytes and triggering release of atrial natriuretic peptide, which promotes natriuresis and opposes further volume gain. Pressure natriuresis contributes as well. Renin is indeed suppressed in primary hyperaldosteronism, but that does not produce the escape phenomenon, and cortisol does not competitively block the mineralocorticoid receptor in normal circumstances because 11-beta-HSD2 inactivates it in the distal nephron.

Reference: Ganong Review of Medical Physiology, 26th ed.

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