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Vascular smooth muscle cells (VSMCs) regulate blood vessel diameter, controlling blood pressure and flow. The nitric oxide (NO)-cGMP pathway is a crucial signaling mechanism for VSMC relaxation. NO, produced by endothelial cells, activates soluble guanylate cyclase (sGC) in VSMCs, leading to cGMP synthesis. cGMP activates protein kinase G (PKG), which reduces intracellular calcium levels and desensitizes contractile machinery, resulting in vasodilation. cGMP is degraded by phosphodiesterases (PDEs). This pathway is a target for drugs treating cardiovascular diseases, including hypertension and erectile dysfunction.
Increased NO availability, increased cGMP levels, activation of PKG, decreased intracellular calcium, desensitization of contractile machinery
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