A patient on oral clonidine for hypertension abruptly stops the drug and presents two days later with blood pressure of 200/120 mmHg, sweating, anxiety, and tachycardia. The basis for this rebound hypertension is:

• A Cross-tolerance with endogenous catecholamines at peripheral vascular receptors
• B Accumulation of norepinephrine in nerve terminals during treatment with abrupt release on withdrawal
• C Supersensitivity of presynaptic alpha-2 autoreceptors leading to exaggerated feedback inhibition reversal
• D Upregulation of postsynaptic alpha-1 receptors during treatment with sudden loss of central sympatholysis ✓

Explanation

Clonidine is a central alpha-2 agonist that reduces sympathetic outflow. Chronic use leads to upregulation of postsynaptic adrenergic receptors. On sudden withdrawal, central sympatholysis disappears while the upregulated receptors produce an overshoot: rebound hypertension often exceeding pretreatment values, with tachycardia and sweating. Treatment involves restarting clonidine or using labetalol or alpha plus beta blockade. Beta-blocker monotherapy can worsen the crisis by removing peripheral beta-2 mediated vasodilation.

Reference: Katzung Basic and Clinical Pharmacology, 16th ed.

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