A patient taking a non-selective beta-blocker for hypertension develops significant bradycardia and bronchospasm during an asthma attack. Blocking which specific receptor subtype accounts for the bronchospasm?

• A Beta-1 adrenoceptors on bronchial smooth muscle
• B Alpha-1 adrenoceptors on airway mucosa causing vasoconstriction and oedema
• C Beta-2 adrenoceptors on bronchial smooth muscle, preventing sympathetically-mediated bronchodilation ✓
• D Muscarinic M3 receptors being unmasked without beta-2 balance

Explanation

Bronchial smooth muscle expresses predominantly beta-2 adrenoceptors. Endogenous catecholamines (adrenaline) maintain baseline bronchodilatation via beta-2 stimulation, which is particularly important during bronchoconstriction. Non-selective beta-blockers (propranolol, carvedilol) block beta-2 receptors in the bronchi, preventing this protective bronchodilatation and potentiating bronchoconstriction. This is why beta-1-selective blockers (metoprolol, bisoprolol) are preferred when beta-blockade is necessary in asthmatic patients, though none are completely safe.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.