Which receptor subtype mediates bronchodilation when a selective beta-2 agonist is inhaled, and what is the intracellular second messenger responsible?

• A Beta-2 receptor; Gs-protein activates adenylyl cyclase → ↑cAMP → PKA phosphorylates MLCK → smooth muscle relaxation ✓
• B Beta-2 receptor; Gi-protein inhibits phospholipase C → ↓IP3 → reduced intracellular Ca2+
• C Alpha-2 receptor; Gs-protein raises cAMP → bronchial smooth muscle hyperpolarisation
• D Beta-1 receptor; cAMP activates protein kinase G → myosin light chain dephosphorylation

Explanation

Beta-2 adrenergic receptors predominate in bronchial smooth muscle. Activation couples via Gs protein to adenylyl cyclase, raising intracellular cAMP. Elevated cAMP activates protein kinase A (PKA), which phosphorylates myosin light chain kinase (MLCK), reducing its activity, and also activates large-conductance Ca2+-activated K+ channels (BKCa), hyperpolarizing the cell. Both effects reduce smooth muscle tone, causing bronchodilation. This is the mechanism of action of salbutamol (albuterol) and salmeterol.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.