Clonidine exerts its antihypertensive effect primarily by acting as an agonist at which receptor subtype, and what is the consequence of abrupt withdrawal?

• A Beta-1 receptors; rebound tachycardia and heart failure
• B Imidazoline I1 receptors only; no rebound effects
• C Alpha-1 postsynaptic receptors; reflex bradycardia upon withdrawal
• D Alpha-2 presynaptic receptors; rebound hypertension due to catecholamine surge ✓

Explanation

Clonidine primarily acts as an alpha-2 agonist at presynaptic receptors in the nucleus tractus solitarius (medullary vasomotor center), reducing sympathetic outflow. It also acts on imidazoline I1 receptors, contributing to its antihypertensive effect. Abrupt withdrawal leads to a rebound catecholamine surge (norepinephrine release from previously inhibited nerve terminals), causing severe rebound hypertension, tachycardia, and anxiety — a hypertensive crisis. Beta-1 and alpha-1 receptor actions do not describe clonidine's mechanism, and I1 receptor action alone does not fully explain its effect.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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