Effects of Nitric Oxide on Atherosclerosis

This chapter highlights the role of Nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) and their roles in vascular physiology and pathophysiological development of atherosclerosis. There are three identified nitric oxide synthase (NOS) isoforms: (1) endothelial NOS (eNOS), (2) cytokine-inducible NOS (iNOS), and (3) neuronal NOS (nNOS). Endothelial dysfunction is considered to be an early marker of atherosclerosis and can develop before clinical angiographic or ultrasound evidence of atherosclerotic plaque formation. NO is a potent oxidant produced by both endothelial cells and macrophages. Depending on the source of production, NO can exert both atherosclerotic and protective effects. Therapeutic intervention for atherosclerosis from the standpoint of eNOS can be focused mainly on correcting endothelial dysfunction and eNOS uncoupling. It is important to note that the NO/•O2 - equilibrium is tightly regulated under normal physiological conditions, and that this balance can be disturbed by endothelial dysfunction.