What is the mechanism of action of nitrates such as nitroglycerin in angina treatment?

Nitrates, such as nitroglycerin, primarily function through the release of nitric oxide (NO) within vascular smooth muscle cells. When nitroglycerin is administered, it undergoes biotransformation to produce nitric oxide, which activates guanylate cyclase. This enzyme then increases the levels of cyclic guanosine monophosphate (cGMP) within the smooth muscle cells. The rise in cGMP leads to vascular smooth muscle relaxation, resulting in vasodilation.

This vasodilation primarily affects the venous capacitance vessels, which reduces preload on the heart, leading to decreased myocardial oxygen demand. Additionally, nitrates can dilate coronary arteries, which may enhance blood flow to ischemic areas of the myocardium during angina episodes.

In contrast, mechanisms not involved in nitrates' action include the inhibition of potassium channels, which is not how nitrates exert their effects, and blocking calcium channels in cardiac myocytes, which pertains to calcium channel blockers. Lastly, enhancing adrenergic signaling to increase heart rate is not the primary action of nitrates; this is more aligned with medications that stimulate the sympathetic nervous system. Thus, the correct understanding of nitrates' mechanism of action highlights their role in increasing nitric oxide