DRSP causes fluid retention by blocking which hormone from its receptor?

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Multiple Choice

DRSP causes fluid retention by blocking which hormone from its receptor?

Explanation:
Anti-mineralocorticoid action of drospirenone blocks aldosterone from binding its receptor in the kidney. Aldosterone normally promotes sodium reabsorption and water retention in the collecting ducts by activating the mineralocorticoid receptor, increasing ENaC activity and Na+/K+ ATPase function. When this receptor is blocked, sodium reabsorption decreases and water follows, producing a diuretic effect that reduces fluid retention. The other hormones act through different pathways—Angiotensin II drives aldosterone release rather than blocking its receptor, Vasopressin increases water reabsorption via V2 receptors, and cortisol acts on glucocorticoid receptors—so they don’t explain the anti-mineralocorticoid effect of drospirenone.

Anti-mineralocorticoid action of drospirenone blocks aldosterone from binding its receptor in the kidney. Aldosterone normally promotes sodium reabsorption and water retention in the collecting ducts by activating the mineralocorticoid receptor, increasing ENaC activity and Na+/K+ ATPase function. When this receptor is blocked, sodium reabsorption decreases and water follows, producing a diuretic effect that reduces fluid retention. The other hormones act through different pathways—Angiotensin II drives aldosterone release rather than blocking its receptor, Vasopressin increases water reabsorption via V2 receptors, and cortisol acts on glucocorticoid receptors—so they don’t explain the anti-mineralocorticoid effect of drospirenone.

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