A patient on clonidine for hypertension abruptly stops the drug. The rebound hypertension that follows is primarily due to:
- A Rebound increase in central norepinephrine release after removal of presynaptic alpha-2 agonism ✓
- B Supersensitivity of peripheral alpha-1 adrenoceptors after chronic blockade
- C Reflex tachycardia from abrupt loss of beta-1 blockade
- D Upregulation of angiotensin II receptors in the kidney
Correct answer: A. Rebound increase in central norepinephrine release after removal of presynaptic alpha-2 agonism
Explanation
Clonidine activates presynaptic alpha-2 autoreceptors in the locus coeruleus and brainstem, suppressing central sympathetic outflow. On abrupt withdrawal, this inhibition is removed, causing a surge in central norepinephrine release and marked sympathetic activation, producing rebound hypertension and tachycardia. Peripheral alpha-1 supersensitivity is not the primary mechanism in this setting.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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