A 42-year-old man with resistant hypertension is started on oral minoxidil. Within weeks he develops marked reflex tachycardia and fine facial hair growth. The antihypertensive mechanism of minoxidil involves:
- A Opening of ATP-sensitive potassium channels in vascular smooth muscle ✓
- B Blockade of L-type calcium channels in arterioles
- C Central alpha-2 receptor agonism reducing sympathetic outflow
- D Inhibition of aldosterone synthesis at the zona glomerulosa
Explanation
Minoxidil sulfate opens ATP-sensitive potassium channels in vascular smooth muscle, causing membrane hyperpolarization, closure of voltage-gated calcium channels, and profound arteriolar vasodilation. The fall in blood pressure triggers intense reflex sympathetic activation, producing tachycardia, fluid retention, and pericardial effusion risk, so it is always combined with a beta-blocker and a diuretic. Hypertrichosis occurs because the same potassium channel opening affects follicular cells. Calcium channel blockade is the mechanism of nifedipine, not minoxidil.
Reference: Katzung's Basic and Clinical Pharmacology, 15th ed.
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