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AT1R基因多态性与福辛普利降压疗效的关系 被引量:1

The relationship of polymorphism of angiotensin Ⅱ receptor 1 gene and the effect of Fosinopril
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摘要 目的研究血管紧张素Ⅱ受体1(AngiotensionⅡ Receptor 1,AT1R)A1166 C多态性与福辛普利降压效果及其对肾素-血管紧张素-醛固酮系统(RAAS)的影响的关系。方法对100例汉族原发性高血压(EssentialHypertension,EH)患者给予福辛普利10 mg/d治疗,并进行AT1R基因A1166C多态性分析,观察不同基因型组治疗前后诊所血压2、4 h动态血压、血浆肾素活性、血管紧张素Ⅱ(AngiotensionⅡ,AⅡ)、醛固酮(Aldosterone,ALD)水平的变化。结果不同AT1R基因型组间的降压指标差异均不显著;血浆肾素活性、AⅡ、ALD变化亦无显著差异。结论EH患者的AT1R基因分型对福辛普利的降压效果及其对RAAS的阻断均无影响。 Objective To study the relationship of polymorphism of Angiotensin Ⅱ Receptor 1 (AT1R) gene and the influences of Fosinopril to the changes of blood pressure , the changes of renin-angiotensin-aldosterone system(RAAS). Methods One hundred mild to moderate essential hypertension(EH) patients were enrolled in this study. Their AT1R gene A1166C polymorphism together with clinic blood pressure, changes before and 4 weeks after treatment with Angiotensin Ⅰ(AⅠ), Angiotensin Ⅱ (A Ⅱ ), Aldosterone (ALD) were investigated. Results There was no significant difference in BP decreasing between AT1R-AA group and AT1R-AC group. The changes of AI, AⅡ ALD between AT1R-AA group and AT1R-AC group had no significant difference. Conclusion Under the treatment of Fosinopril, there are no significant differences in the decrease of BP and the block of RAAS between AT1R-AA group and AT1R-AC group.
出处 《同济大学学报(医学版)》 CAS 2007年第3期69-71,共3页 Journal of Tongji University(Medical Science)
关键词 血管紧张素Ⅱ受体1基因 福辛普利 原发性高血压 肾素-血管紧张素-醛固酮系统 angiotensin ⅡReceptor 1 Gene fosinopril essential hypertension renin-angiotensin-aldosterone system
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  • 2Spiering W,Zwaan IM,Kroon AA,et al.Genetic influences on 24 h blood pressure profiles in a hypertensive population:role of the angiotensin-converting enzyme insertion/deletion and angiotensin Ⅱ type 1 receptor A1166C gene polymorphisms[J].Blood Press Monit,2005,10(3):135-141.
  • 3Sugimoto K,Katsuya T,Ohkubo T,et al.Association between angiotensin Ⅱ type 1 receptor gene polymorphism and essential hypertension:the Ohasama Study[J].Hypertens Res,2004,27(8):551-556.
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