Nitroglycerin is a nitrate vasodilator used to treat or prevent angina, treat hypertension, control heart failure in myocardial infarction, and to induce hypotension intraoperatively. Nitroglycerin is converted by mitochondrial aldehyde dehydrogenase (mtALDH) to nitric oxide (NO). NO activates the enzyme guanylate cyclase. The activation of this enzyme is followed by the synthesis of cyclic guanosine 3',5'-monophosphate (cGMP), activating a cascade of protein kinase-dependent phosphorylation events in smooth muscles, ultimately resulting in the dephosphorylation of myosin light chains within smooth muscle fibers. This activity causes the relaxation of smooth muscle within blood vessels, resulting in the desired vasodilatory effect. Although nitroglycerin has a vasodilatory effect in both arteries and veins, the profound desired effects caused by nitroglycerin are primarily due to venodilation. Venodilation causes pooling of blood within the venous system, reducing preload to the heart, which causes a decrease in cardiac work, reducing anginal symptoms secondary to demand ischemia. Arterial vasodilation will still occur and contribute towards the relief of anginal symptoms, but its effects are not as significant. Vasodilation of the coronary arteries will cause increased blood flow to the heart, increasing perfusion, but this effect remains minimal compared to the effects of venodilation.

Nitroglycerin Pathway References