Nitric oxide (NO) produced by vascular endothelial cells causes vasodilation. Which intracellular mechanism mediates smooth muscle relaxation?

• A NO activates soluble guanylyl cyclase → cGMP → PKG → dephosphorylates myosin light chain → relaxation ✓
• B NO inhibits voltage-gated calcium channels reducing intracellular Ca2+ → smooth muscle relaxation
• C NO activates adenylyl cyclase → cAMP → PKA → myosin light chain kinase inhibition → relaxation
• D NO directly hyperpolarizes smooth muscle cells by activating large-conductance BKCa channels

Explanation

The canonical NO-cGMP signaling pathway: NO (a small lipophilic gaseous molecule) diffuses from endothelial cells into vascular smooth muscle cells, where it directly activates soluble guanylyl cyclase (sGC). sGC converts GTP to cGMP. cGMP activates protein kinase G (PKG), which phosphorylates myosin light chain phosphatase (MLCP) — increasing its activity — and other targets, resulting in dephosphorylation of myosin light chains and smooth muscle relaxation. Options B and D are secondary downstream effects that can occur but are not the primary mechanism. Option C describes the prostacyclin (PGI2) pathway, not NO.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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