P. Lacolley et al., NITRIC-OXIDE SYNTHASE GENE POLYMORPHISMS, BLOOD-PRESSURE AND AORTIC STIFFNESS IN NORMOTENSIVE AND HYPERTENSIVE SUBJECTS, Journal of hypertension, 16(1), 1998, pp. 31-35
Background Genetic studies may help us to understand the mechanisms un
derlying the involvement of various neuro-humoral factors in the regul
ation of the mechanical properties of large arteries. We have shown pr
eviously 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 nit
ric oxide synthase gene to aortic stiffness in normotensive and hypert
ensive subjects in the same cohort. Methods We studied 309 untreated h
ypertensive and 123 normotensive subjects. Aortic stiffness was evalua
ted by measuring the carotid-femoral pulse-wave velocity non-invasivel
y. 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 determ
ined in each subject. Results The distributions of genotypes and allel
e prevalences of the endothelial nitric-oxide synthase G(10)-T polymor
phisms among hypertensive and normotensive subjects were similar. In c
ontrast, the prevalence of the nitric oxide synthase (298)G allele was
higher in the hypertensive group than it was among normotensive subje
cts. 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 c
ommon polymorphisms of the endothelial nitric oxide synthase gene are
involved in the regulation of aortic stiffness in hypertensive and nor
motensive individuals. The higher prevalence of endothelial nitric oxi
de synthase (298)G allele among hypertensives suggests that this gene
is involved in essential hypertension but this observation needs furth
er confirmation. (C) 1998 Rapid Science Ltd.