Beta-2 adrenergic receptors in skeletal muscle blood vessels cause vasodilation. This response is mediated by:

• A Gi-coupled inhibition of phospholipase C, reducing IP3 and DAG, preventing smooth muscle contraction
• B Gs-coupled activation of adenylyl cyclase, raising cAMP which activates PKA to phosphorylate and inhibit myosin light-chain kinase (MLCK) in vascular smooth muscle ✓
• C Beta-2 receptor activation of eNOS in endothelial cells, increasing NO production and causing vasodilation
• D Beta-2 receptor stimulation of K+ channels in smooth muscle, causing hyperpolarisation and vasodilation

Explanation

Beta-2 adrenergic receptors are Gs-protein coupled, activating adenylyl cyclase to increase cAMP. Elevated cAMP activates protein kinase A (PKA), which phosphorylates myosin light-chain kinase (MLCK) at an inhibitory site, reducing its activity. Since MLCK is required to phosphorylate myosin light chains and initiate smooth muscle cross-bridge formation, its inhibition leads to smooth muscle relaxation and vasodilation. This mechanism also underlies bronchodilation (beta-2 agonists in asthma) and uterine relaxation (tocolysis). Options B–D describe alternative mechanisms that are not the primary beta-2 vasodilatory pathway in skeletal muscle vasculature.

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

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