Abstract
Genetic variants of eNOS gene play a significant role in the pathogenesis of hypertension. Many environmental factors have, also, been implicated in the aetiology of hypertension. We carried out an age-matched case-control study among adults. Hypertension was defined according to JNC-VII criteria and eNOS gene polymorphisms were determined by PCR and PCR followed by PCR-RFLP. eNOS intron 4 aa genotype (adjusted OR 6.81; 95% CI 2.29–20.25) and eNOS 894TT genotype (adjusted OR 7.84; 95% CI 2.57–23.96) were associated with the risk of hypertension. Tobacco users (either smoking/chewing or both) with eNOS intron 4 aa genotype (OR 14.00: 95% CI 1.20–163.37), eNOS 894GG genotype (OR 5.56: 95% CI 3.72–8.31), and eNOS T-786C CC genotype (OR 9.00: 95% CI 1.14–71.04) were at an increased risk of hypertension. Similarly a significant gene-environment interaction was observed between individuals consuming alcohol with eNOS intron 4 aa genotype (OR 12.00: 95% CI 1.20–143.73) and eNOS 894GG genotype (OR 1.95: 95% CI 1.35–2.81). The present study identified few susceptible genotypes of the eNOS gene with the risk of hypertension. Moreover, the interactive effects between the environmental factors and the risk of hypertension were dependent on the eNOS genotypes.
Highlights
Nitric oxide (NO) produced from L-arginine by endothelial nitric oxide synthase plays a significant role in the regulation of vascular tone and in the control of blood pressure [1]
Genotype and allelic frequencies for the endothelial nitric oxide synthase (eNOS) gene polymorphisms for eNOS gene intron 4 ab polymorphism and eNOS gene exon 7 Glu298Asp variant were in agreement with the frequencies predicted by the Hardy-Weinberg equilibrium (χ2 = 1.12, df = 2, P > 0.05 and χ2 = 2.67, df = 2, P > 0.05, resp.)
In multivariate model of logistic regression too, the risk persisted even after adjustment for age, sex, extra salt intake, smoking, tobacco chewing, and habit of alcohol consumption (eNOS intron 4 aa genotype and eNOS intron 4 ab genotype)
Summary
Nitric oxide (NO) produced from L-arginine by endothelial nitric oxide synthase (eNOS) plays a significant role in the regulation of vascular tone and in the control of blood pressure [1]. The complex interplay between the environmental factors and genes for the risk of hypertension is still not clear and many dietary and lifestyle factors have been implicated in the aetiology of hypertension In earlier studies, both tobacco use (either smoking/chewing or both) and alcohol consumption were associated with an increased risk of hypertension [8,9,10]. The same study calculated the population attributable risk (PAR) and were found to be 70.3% (95% CI 63.0–77.5) for tobacco use, 45.3% (95% CI 37.1–53.4) for tobacco chewing, 31.5% (95% CI 21.3–40.9) for smoking, and 33.6% (95% CI 22.9–44.4) for alcohol consumption This prompted us to conduct an investigation to study the association between the polymorphisms of the endothelial nitric oxide synthase gene and hypertension in the tea garden worker community of northeastern India where the prevalence of hypertension is high [12]
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