A hypertensive man abruptly stops his clonidine tablets. Two days later he presents with blood pressure of 210/120 mmHg, sweating, anxiety, and tachycardia. The mechanism of this rebound phenomenon is:
- A Loss of central alpha-2 agonist suppression of sympathetic outflow, with supersensitive postsynaptic responses to circulating catecholamines ✓
- B Upregulation of beta-adrenergic receptors during therapy
- C Accumulation of clonidine metabolites acting as antagonists
- D Volume expansion from mineralocorticoid excess
Correct answer: A. Loss of central alpha-2 agonist suppression of sympathetic outflow, with supersensitive postsynaptic responses to circulating catecholamines
Explanation
Clonidine stimulates central alpha-2B receptors in the brainstem, reducing sympathetic discharge. Chronic use leads to adaptive changes including downregulation of these receptors; abrupt withdrawal removes central inhibition while catecholamine levels are elevated, producing rebound hypertension above baseline, often with tachycardia and agitation. Treatment is reinstitution of clonidine or an alpha-beta blocker such as labetalol.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
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