Nitric oxide synthase gene polymorphisms, blood pressure and aortic stiffness in normotensive and hypertensive subjects

Background Genetic studies may help us to understand the mechanisms underlying the involvement of various neuro-humoral factors in the regulation of the mechanical properties of large arteries. We have shown previously that the angiotensin II type 1 receptor gene polymorphism was a strong determinant of aortic stiffness in hypertensives. Objective To assess the contribution of two polymorphisms of the endothelial nitric oxide synthase gene to aortic stiffness in normotensive and hypertensive subjects in the same cohort. Methods We studied 309 untreated hypertensive and 123 normotensive subjects. Aortic stiffness was evaluated by measuring the carotid-femoral pulse-wave velocity non-invasively. The endothelial nitric oxide synthase gene polymorphisms G(10)-T at intron 23 (G(IN23)T) and G(298)-T at exon 7 (Glu(298)Asp) were determined in each subject. Results The distributions of genotypes and allele prevalences of the endothelial nitric-oxide synthase G(10)-T polymorphisms among hypertensive and normotensive subjects were similar. In contrast, the prevalence of the nitric oxide synthase (298)G allele was higher in the hypertensive group than it was among normotensive subjects. We found no association of the endothelial nitric oxide synthase genotypes with blood pressure levels or pulse-wave velocity for either population. Conclusions The present results do not suggest that two common polymorphisms of the endothelial nitric oxide synthase gene are involved in the regulation of aortic stiffness in hypertensive and normotensive individuals. The higher prevalence of endothelial nitric oxide synthase (298)G allele among hypertensives suggests that this gene is involved in essential hypertension but this observation needs further confirmation. (C) 1998 Rapid Science Ltd.