Nitric oxide (NO), an unstable derived of nitrogen, is released by endothelium in response to physiological stimulus. Indeed, the endothelium is not only a barrier between the lumen and the inner side of the vessel wall but also a metabolically active organ with endocrine, paracrine and autocrine functions. Endothelial vascular cells play an important role in the regulating vasomotor tone, local homeostasis and vascular bed proliferation. NO mediates the vasodilation and inhibits platelet aggregation, expression of molecular adhesion of monocyte, neutrophils adhesion and smooth muscle growth. Atherosclerosis risk factors such as hypercholesteremia, high blood pressure, smoking and oxidative stress inhibit NO production, leading paradoxically to vasodilatation, which affects endothelial function and may lead to ischemic manifestations in patients with arterial pathology. Therapies that increase NO production may improve endothelial vasodilatation. To check whether a decrease or lower production of NO terminates with the initial formation of atheromatous plaque or whether it continues, we determined the content of NO in plasma and plaque of subjects undergoing carotid surgery and in plasma of control subjects.