A 35-year-old woman with an aldosterone-producing adenoma has hypertension, serum potassium of 2.8 mEq/L, and venous bicarbonate of 34 mEq/L. The mechanism of her metabolic alkalosis is best explained by:
- A Aldosterone-stimulated hydrogen ion secretion by alpha-intercalated cells coupled to sodium reabsorption ✓
- B Volume depletion causing bicarbonate retention in the proximal tubule
- C Direct action of aldosterone on the bicarbonate buffer system in plasma
- D Potassium movement out of cells exchanging with hydrogen ions entering cells
Correct answer: A. Aldosterone-stimulated hydrogen ion secretion by alpha-intercalated cells coupled to sodium reabsorption
Explanation
Aldosterone acts on principal cells to increase ENaC-mediated sodium reabsorption, generating a lumen-negative potential that drives hydrogen ion secretion by alpha-intercalated cells via H-ATPase, along with potassium secretion. The resulting loss of both H+ and K+ produces hypokalaemic metabolic alkalosis. Intracellular potassium-hydrogen exchange does occur in hypokalaemia but is a secondary contributor, not the primary renal mechanism here.
Reference: Ganong's Review of Medical Physiology, 26th ed.
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