Assessment of the role of plasma nitric oxide levels, T?786C genetic polymorphism, and gene expression levels of endothelial nitric oxide synthase in the development of coronary artery disease

Reduced bioavailability of nitric oxide (NO) and the T?786C polymorphism of endothelial nitric oxide synthase (eNOS) gene have been reported as risk factors for the development of coronary artery disease (CAD) with conflicting results. We investigated the association of plasma NO levels, T?786C genetic polymorphism, and gene expression levels of eNOS with CAD risk in an Iranian subpopulation.
Studied population included 100 patients with angiographically verified CAD and 100 ethnically matched controls. Analysis of T?786C genetic polymorphism and gene expression levels of eNOS was conducted by polymerase chain reaction (PCR) restriction fragment length polymorphism and real?time reverse transcription?PCR methods, respectively. Plasma levels of NO were measured using Griess method.
The CC genotype distribution (15% vs. 6%, P = 0.011) and minor C allele frequency (36.5% vs. 21.5%, P = 0.001) of eNOS T?786C polymorphism differed significantly between CAD patients and control. Furthermore, eNOS T?786C polymorphism was more common among smoker than nonsmoker CAD patients (27.7% vs. 7.8%, P = 0.044). The association of the eNOS T?786C polymorphism with the severity of CAD (number of diseased vessel) was significant (P Our study indicated that reduced NO levels and eNOS T?786C genetic polymorphism are significant risk factors for the development and severity of CAD in the Iranian population.