Nitric oxide (NO) is a pivotal signaling messenger in the cardiovascular system. NO participates in regulatory functions including control of hemostasis, fibrinolysis, platelet and leukocyte interactions with the arterial wall, regulation of vascular tone, proliferation of vascular smooth muscle cells, and homeostasis of blood pressure. Diminished NO bioavailability and abnormalities in NO-dependent signaling are among central factors of vascular disease, although it is unclear whether this is a cause of, or result of endothelial dysfunction or both pathogenic events. Disturbances in NO bioavailability have been linked to cause endothelial dysfunction, leading to increased susceptibility to atherosclerotic lesion progression, hypertension, hypercholesterolemia, diabetes mellitus, thrombosis and stroke.