A patient taking a non-selective beta-blocker develops paradoxical severe hypertension after receiving epinephrine for an anaphylactic reaction. Which mechanism best explains this paradox?
- A Beta-blockers enhance release of norepinephrine from adrenal medulla
- B Non-selective beta-blockers activate alpha-1 receptors directly
- C Beta-blockade prevents epinephrine-mediated vasodilation via beta-2 receptors, leaving unopposed alpha-1 mediated vasoconstriction ✓
- D Epinephrine's alpha-2 agonism is enhanced in the presence of beta-blockade
Explanation
Epinephrine stimulates both alpha (vasoconstriction) and beta-2 (vasodilation) adrenoceptors. Normally the vasodilatory beta-2 effect attenuates the alpha-mediated pressor response. When non-selective beta-blockers are present, beta-2 vasodilation is blocked while alpha-1-mediated vasoconstriction is fully expressed, resulting in paradoxical severe hypertension and reflex bradycardia. This clinically significant interaction means selective beta-1 blockers are safer in patients who may need epinephrine, and glucagon is the preferred treatment for beta-blocker overdose.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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