A 45-year-old woman is investigated for hypertension, hypokalemia, and low plasma renin activity. CT abdomen shows a 1.8 cm right adrenal adenoma. Adrenal vein sampling confirms autonomous aldosterone hypersecretion from the right adrenal. What is the pathological mechanism of hypertension in Conn's syndrome?

• A Autonomous aldosterone secretion causes sodium and water retention, expanding plasma volume and suppressing renin, leading to hypertension and hypokalemia ✓
• B Excess aldosterone stimulates cortisol receptors, causing Cushing-like hypertension
• C Aldosterone excess activates RAAS through angiotensin II feedback, amplifying vasoconstriction
• D Excess aldosterone increases renal prostaglandin synthesis, causing renal vasoconstriction

Explanation

In primary hyperaldosteronism (Conn's syndrome), autonomous aldosterone secretion from an adrenal cortical adenoma acts on the mineralocorticoid receptor in collecting duct principal cells, causing sodium reabsorption and potassium/hydrogen ion excretion. Sodium retention expands extracellular fluid and plasma volume, raising blood pressure while suppressing renin (unlike secondary hyperaldosteronism where renin is elevated). Hypokalemia results from obligatory urinary potassium loss driven by the aldosterone-mediated sodium-potassium exchange.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

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