A patient receiving clonidine for hypertension abruptly stops the medication. Within 18 hours, blood pressure rises to 210/120 mmHg. The mechanism of this rebound hypertension is:
- A Upregulation of beta-1 adrenergic receptors in the heart
- B Supersensitivity of central alpha-2 receptors and catecholamine surge following removal of inhibition ✓
- C Upregulation of peripheral alpha-2 receptors causing excess norepinephrine release
- D Loss of direct vasodilatory effect of clonidine on blood vessels
Explanation
Clonidine acts centrally on alpha-2 receptors in the nucleus tractus solitarius to reduce sympathetic outflow. With chronic use, postsynaptic and presynaptic alpha-2 receptors are upregulated (supersensitized). On abrupt withdrawal, the sympathetic system is no longer suppressed and there is an exaggerated catecholamine surge, resulting in severe rebound hypertension, sweating, and anxiety. This is why clonidine should always be tapered gradually, and the rebound is treated with restarting clonidine or combined alpha-beta blockade.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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