A 38-year-old man has hypertension, hypokalemia (K+ 2.8 mEq/L), and metabolic alkalosis. Plasma renin activity (PRA) is suppressed and plasma aldosterone is elevated. 24-hour urine aldosterone is 40 μg (elevated). Which physiological concept explains the hypokalemia in this case?

• A Excess aldosterone suppresses the adrenal zona glomerulosa, reducing cortisol which normally retains potassium
• B Excess aldosterone acts on ENaC in the cortical collecting duct to retain Na+ in exchange for K+ secretion via ROMK channels ✓
• C Hypertension causes glomerular hyperfiltration, washing out potassium in the tubules
• D Suppressed renin causes reduced angiotensin II, reducing Na+/K+ ATPase activity in the proximal tubule

Explanation

Primary hyperaldosteronism (Conn's syndrome): excess autonomous aldosterone acts on mineralocorticoid receptors in the principal cells of the cortical collecting duct, upregulating ENaC (epithelial Na+ channels) on the apical membrane and Na+/K+ ATPase on the basolateral membrane. This drives Na+ reabsorption, creating a lumen-negative potential difference that drives K+ secretion through ROMK (apical K+ channels) and Cl− secretion. The resulting urinary K+ wasting causes hypokalemia and metabolic alkalosis (H+ also secreted to maintain electroneutrality). Suppressed PRA confirms the autonomous aldosterone source is not renin-angiotensin mediated.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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