A patient with cirrhosis and refractory ascites is given tolvaptan. Its mechanism differs from all other diuretics because:
- A Tolvaptan is a vasopressin V2 receptor antagonist (vaptans), causing aquaresis — excretion of electrolyte-free water — without increasing urinary sodium excretion ✓
- B Tolvaptan inhibits aldosterone at the mineralocorticoid receptor, causing sodium excretion without potassium loss
- C Tolvaptan inhibits carbonic anhydrase in the collecting duct, causing bicarbonate diuresis
- D Tolvaptan activates aquaporin-2 channels constitutively, causing water reabsorption from the tubule
Explanation
Tolvaptan is a selective V2 (vasopressin-2) receptor antagonist; by blocking AVP (ADH) action on renal collecting duct principal cells, it prevents cAMP-mediated aquaporin-2 insertion, causing excretion of large volumes of dilute (electrolyte-free) urine — termed 'aquaresis' — distinct from the natriuretic diuresis of loop/thiazide diuretics. This is particularly useful for hyponatremia and hypervolemic states. All other diuretic classes promote sodium (and thus water) excretion, altering electrolyte balance.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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