A 45-year-old hypertensive man stops clonidine abruptly on his own. Three days later he presents with blood pressure of 220/130 mmHg, palpitations, sweating, and headache. The mechanism of this presentation is best described as:
- A Supersensitivity of postsynaptic alpha-1 receptors with loss of central alpha-2 agonism, causing catecholamine surge ✓
- B Accumulation of the active metabolite of clonidine causing paradoxical vasoconstriction
- C Rebound volume expansion due to aldosterone escape
- D Unmasking of phaeochromocytoma previously suppressed by clonidine
Correct answer: A. Supersensitivity of postsynaptic alpha-1 receptors with loss of central alpha-2 agonism, causing catecholamine surge
Explanation
Clonidine is a central alpha-2 adrenergic agonist that suppresses sympathetic outflow from the vasomotor centre. Abrupt withdrawal removes this suppression while upregulated postsynaptic adrenergic responsiveness persists, producing overshoot hypertension, tachycardia, sweating and anxiety resembling phaeochromocytoma. Treatment is reinstitution of clonidine or an alpha-beta blocker such as labetalol. Aldosterone escape and occult tumour are not the mechanism, though clonidine was historically used as a suppression test.
Reference: Katzung Basic and Clinical Pharmacology, 15th ed.
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