A hypertensive patient stops taking clonidine abruptly after several years of therapy. Two days later he presents with headache, sweating, tremor, and blood pressure of 210/120 mmHg. The mechanism underlying this rebound phenomenon is:
- A Accumulation of circulating catecholamines that were previously degraded by MAO
- B Loss of central alpha-2 agonist effect with upregulated adrenergic signaling causing overshoot sympathetic discharge ✓
- C Volume expansion secondary to mineralocorticoid escape
- D Autoantibody-mediated activation of peripheral alpha-1 receptors
Correct answer: B. Loss of central alpha-2 agonist effect with upregulated adrenergic signaling causing overshoot sympathetic discharge
Explanation
Clonidine is a central alpha-2 agonist that suppresses sympathetic outflow from the vasomotor center. Chronic use leads to adaptive changes, and abrupt withdrawal removes this restraint, producing a surge of catecholamine release with hypertension, tachycardia, sweating, and anxiety resembling pheochromocytoma. Treatment is reinstitution of clonidine or use of alpha and beta blockers such as labetalol. Volume expansion plays no role in this acute event.
Reference: Katzung Basic and Clinical Pharmacology, 15th ed.
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