A patient on a non-selective beta-blocker develops paradoxical hypertension after receiving epinephrine for an anaphylactic reaction. Which adrenoceptor subtype interaction best explains this phenomenon?
- A Beta-blocker causes direct stimulation of alpha-2 receptors
- B Blockade of beta-2 receptors unmasks alpha-1 mediated vasoconstriction from epinephrine ✓
- C Epinephrine binds preferentially to alpha-2 presynaptic receptors causing norepinephrine release
- D Non-selective beta-blockade enhances M2 muscarinic receptor sensitivity
Explanation
Non-selective beta-blockers (propranolol, nadolol) block both beta-1 and beta-2 receptors. When epinephrine is given, its vasodilatory beta-2 effect on skeletal muscle vessels is eliminated, leaving unopposed alpha-1 vasoconstriction. This paradoxically raises blood pressure, worsening anaphylaxis management. This is why selective beta-1 blockers or glucagon (which bypasses adrenoceptors) are preferred in beta-blocker-treated patients with anaphylaxis.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.