首都医科大学学报 ›› 2006, Vol. 27 ›› Issue (2): 226-229.

• 临床研究 • 上一篇    下一篇

内皮型一氧化氮合酶基因T786C多态性与原发性高血压的相关关系

李东宝, 华琦, 皮林   

  1. 首都医科大学宣武医院心血管内科
  • 收稿日期:2004-06-16 修回日期:1900-01-01 出版日期:2006-04-24 发布日期:2006-04-24
  • 通讯作者: 华琦

The Relationship of T786C Polymorphism of Endothelial Nitric Oxide Synthase Gene to Essential Hypertension

Li Dongbao, Hua Qi, Pi Lin   

  1. Department of Cardiology, Xuanwu Hospital, Capital University of Medical Sciences
  • Received:2004-06-16 Revised:1900-01-01 Online:2006-04-24 Published:2006-04-24

摘要: 目的 探讨内皮型一氧化氮合酶(eNOS)基因T786C多态性与中国汉族人原发性高血压(EH)的相关性.方法 采用多聚酶链式反应(PCR)结合限制性内切酶片段长度多态分析方法,检测167例健康人和267例高血压患者的eNOS基因T786C多态性,并用硝酸还原酶法测定空腹血清一氧化氮代谢物(NOx)水平,用放射免疫法测定内皮素(ET)的浓度.结果 EH组CT+CC基因型和C等位基因频率显著高于对照组(P<0.05);TT基因型的空腹血清NOx浓度[(77.68±33.36)μmol/L]、NOx/ET比(1.41±1.28)明显高于CT+CC基因型[(67.15±24.22)μmol/L、0.93±0.51](P<0.05);TT基因型ET水平[(68.70±29.04)ng/L]明显低于CT+CC基因型[(78.23±31.17)ng/L](P<0.05).结论 eNOS基因T786C多态性的C等位基因与中国汉族人EH的发生相关,C等位基因携带者可能通过减少内皮NO的释放参与EH发病.

关键词: 原发性高血压, 一氧化氮合酶, 多态性, 一氧化氮

Abstract: Objective To investigate the relationship of the T786C polymorphism of endothelial nitric oxide synthase(eNOS) gene to essential hypertension(EH) in Chinese population.Methods Polymerase chain reaction combined with restriction enzyme digestion was used to detect the polymorphism of eNOS gene in 167 normotensive subjects controls and 267 hypertensive patients;Fasting serum nitric oxide metabolite(NOx) and Endothelin(ET) were measured by nitrate reductase and radioimmunoassay respectively.Results 1) The frequencies of C allele and CC+CT genotype in EH were significantly higher than those in control group(P<0.01);2) The level of NOx and the rate of NOx/ET were higher in TT genotype [(77.68±33.36)μmol/L,1.41±1.28] than those in CT+CC genotype [(67.15±24.22)μmol/L,0.93±0.51] of EH.The level of ET were lower in TT genotype [(68.70±29.04)ng/L] than in CT+CC genotype [(78.23±31.17)ng/L] of EH.Conclusion It is suggested that the T786C pollymorphism of eNOS gene is reltated to EH in Chinese population.C allele may be involved in the etiology of EH by reducing NO release of endothelium.

Key words: essential hypertension, nitric oxide synthase, polymorphism, nitric oxide

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