Nitric Oxide (NO) plays an important role in the vascular system by inducing vasodilation, regulating blood flow and blood pressure, and conferring thrombo-resistance and protective properties to the endothelium of blood vessels. Endothelium-dependent vasodilation is mediated by the release of NO produced by endothelial oxide synthetase (eNOS). A reduced synthesis of NO or its lower bio-availability could be the cause of the reduced endothelium-dependent vasodilatation that is observed in the blood vessels of subjects with cardiovascular risk factors, such as active and passive smokers, patients with hypertension or hypercholesterolemia. The lack of NO-mediated effects can also predispose to the development of atherosclerosis. The -786 T> C polymorphism of the promoter region of the gene encoding endothelial oxide synthetase (NOS3) reduces endothelial NO synthesis, suggesting that patients carrying this nucleotide variation are predisposed to cardiovascular coronary disease onset. The major indication is given by the fact that this reduction is exacerbated by cigarette smoking. Analysis of the -786 T> C polymorphism is carried out by gene amplification (PCR) of the NOS3 gene and automated fluorescence-based DNA sequence analysis.