A patient on clonidine for hypertension abruptly stops the drug and develops severe rebound hypertension, sweating, and palpitations within 18 hours. What is the primary mechanism underlying this rebound phenomenon?
- A Sudden loss of central alpha-2 agonism leading to sympathetic overactivity ✓
- B Upregulation of beta-1 receptors in the heart
- C Increased renin release from the juxtaglomerular cells
- D Decreased baroreceptor sensitivity
Correct answer: A. Sudden loss of central alpha-2 agonism leading to sympathetic overactivity
Explanation
Clonidine acts on presynaptic alpha-2 receptors in the nucleus tractus solitarius and locus coeruleus, reducing central sympathetic outflow. Abrupt discontinuation removes this brake, causing a surge in sympathetic activity with marked noradrenaline release — manifesting as rebound hypertension, tachycardia, and sweating. Beta-receptor upregulation is a concern with beta-blocker withdrawal, not clonidine. Renin release plays a secondary role at most.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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