The vasodilatory action of clonidine used in hypertensive emergency (IV) is opposite to its usual antihypertensive effect. This paradoxical pressor response is due to stimulation of:

• A Peripheral alpha-1 receptors on vascular smooth muscle at high concentrations ✓
• B Central alpha-2A receptors in the nucleus tractus solitarius
• C Imidazoline I1 receptors in the rostral ventrolateral medulla
• D Presynaptic alpha-2 receptors causing norepinephrine reuptake inhibition

Explanation

At high IV doses, clonidine can stimulate peripheral vascular alpha-1 adrenoceptors (and peripheral alpha-2B receptors on blood vessels) causing vasoconstriction and a transient pressor response before its central antihypertensive effects dominate. This is why rapid IV administration may cause brief hypertension followed by the expected hypotensive effect. The central alpha-2A effect in the NTS and imidazoline I1 receptor stimulation are responsible for the sustained antihypertensive action, not the initial pressor effect.

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

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