Nitric oxide is an important factor in the regulation of vasodilator tone. In vascular cells, NO is synthesized by endothelial nitric oxide synthase, a key enzyme of the endogenous vasodilator system. Some studies have described the interaction between NO and the other factors that promote vasodilatation in vascular smooth muscular cells. Some of those factors are angiotensin-converting enzyme (ACE), transforming growth factor beta (TGF beta), and endothelial oxide nitric synthase (eNOS). Polymorphism that can alter the expression or the function of the eNOS protein has been identified in the eNOS gene in the promoter and codification zones. We studied the Glu298Asp variant of the eNOS gene in 52 hemodialysis (HD) patients, 22 peritoneal dialysis (PD) patients, and 93 healthy controls. Identification of the Glu298Asp variant in exon 7 was performed by enzymatic amplification and restriction fragment length polymorphism (RFLP) analysis. The frequencies of eNOS genotypes in the control group were GG, 39.8%; GT, 43%; and TT, 17.2%. In HD patients, the frequencies were GG, 40.3%; GT, 38.7%; and TT, 21.7%. In PD patients, they were GG, 41.6%; GT, 50%; and TT, 8.6%. No significant differences were seen between the control group and the dialysis patients, or between the HD and the PD patients.