Vascular smooth muscle cell relaxation via nitric oxide donor activity

Nitric oxide (NO) donors are compounds that deliver NO bioactivity, leading to relaxation of vascular smooth muscle cells (VSMCs). NO activates soluble guanylate cyclase, increasing cGMP, which mediates downstream effects resulting in decreased intracellular calcium and/or reduced myosin light chain phosphorylation, culminating in smooth muscle relaxation and vessel dilation. NO also inhibits proliferation and migration of VSMCs, contributing to the inhibition of atherogenesis. Clinically, this mechanism underlies the vasodilatory effect of drugs like nitroglycerin and sodium nitroprusside, used in the treatment of angina, heart failure, and hypertensive emergencies.

Other names

VSMC relaxation via NO donorsNitric oxide-mediated vasodilationNO donor-induced vasorelaxation

Activation of soluble guanylate cyclase (sGC) by nitric oxide. Increase of cyclic guanosine monophosphate (cGMP) in smooth muscle cells. Activation of protein kinase G (PKG), leading to decreased intracellular calcium and myosin light chain dephosphorylation. Reduced sensitivity to intracellular calcium (alteration in myofilament calcium sensitivity).