Shoji M, Tsutaya S, Saito R, Takamatu H, Yasujima M
Department of Laboratory Medicine, Hirosaki University School of Medicine, Japan.
Life Sci. 2000 May 19;66(26):2557-62. doi: 10.1016/s0024-3205(00)00589-0.
Vascular endothelial cells produce nitric oxide (NO), which contributes to the regulation of blood pressure and regional blood flow. Although Endothelial NO synthase (eNOS) gene polymorphisms have been shown to have a positive association with coronary artery disease, the linkage between eNOS gene polymorphisms and hypertension has been controversial. In the present study, therefore, we identified genotypes for Glu298Asp and variable number tandem repeats in intron 4 (4b/a) in 183 hypertensive and 193 normotensive populations. The Glu298Asp variant had a significant association with hypertension (odds ratio, 1.8; 95% confidence interval, 1.1-3.0). The allele frequencies of 298Asp for Glu298 in hypertensive patients were significantly higher than those in normotensive subjects (0.128 vs 0.080, p<0.05). Diastolic and mean arterial blood pressures were significantly higher in hypertensive subjects with the 298Asp allele than those without the variant allele (p<0.05). However, disequilibrium of 4b/a polymorphism was absent between these two groups. These results suggest that the Glu298Asp variant may be a genetic susceptibility factor for hypertension.
血管内皮细胞产生一氧化氮(NO),其有助于调节血压和局部血流。尽管内皮型一氧化氮合酶(eNOS)基因多态性已被证明与冠状动脉疾病呈正相关,但eNOS基因多态性与高血压之间的联系一直存在争议。因此,在本研究中,我们在183名高血压患者和193名血压正常人群中鉴定了Glu298Asp的基因型以及内含子4(4b/a)中的可变数目串联重复序列。Glu298Asp变异与高血压显著相关(优势比,1.8;95%置信区间,1.1 - 3.0)。高血压患者中Glu298的298Asp等位基因频率显著高于血压正常者(0.128对0.080,p<0.05)。携带298Asp等位基因的高血压患者的舒张压和平均动脉压显著高于不携带该变异等位基因的患者(p<0.05)。然而,两组之间不存在4b/a多态性的不平衡。这些结果表明,Glu298Asp变异可能是高血压的一个遗传易感因素。