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血管紧张素转换酶、血管紧张素原与肥胖:一条导致高血压的潜在途径。

ACE, angiotensinogen and obesity: a potential pathway leading to hypertension.

作者信息

Cooper R, McFarlane-Anderson N, Bennett F I, Wilks R, Puras A, Tewksbury D, Ward R, Forrester T

机构信息

Department of Preventive Medicine and Epidemiology, Loyola University Stritch School of Medicine, Maywood, IL 60153, USA.

出版信息

J Hum Hypertens. 1997 Feb;11(2):107-11. doi: 10.1038/sj.jhh.1000391.

Abstract

The renin-angiotensin system (RAS) plays a crucial role in the regulation of fluid volume, thereby influencing blood pressure (BP). Obesity is an important risk factor for hypertension, however the physiologic basis for this relationship has not been clarified. In a population survey we examined the potential relationship between the RAS and obesity. Based on community sampling, 449 individuals were recruited from metropolitan Kingston, Jamaica. Serum angiotensin-converting enzyme (ACE) and circulating angiotensinogen levels were measured and the associated genes were typed for previously described polymorphisms. Obese individuals (body mass index > 31) had significantly higher serum ACE and angiotensinogen levels, this relationship persisted for ACE in multivariate analyses controlling for BP, hypertension status, age, and gender. The insertion/deletion polymorphism of the ACE gene was associated with variation in the levels of ACE, but inconsistently with body mass index. Variants of the angiotensinogen gene leading to amino acid substitutions at positions 174 and 235 did not influence levels either of angiotensinogen or obesity. These data suggest that obesity may alter the levels of ACE and angiotensinogen, and provide a potential pathway through which obesity leads to elevation of BP.

摘要

肾素-血管紧张素系统(RAS)在调节体液量方面起着关键作用,从而影响血压(BP)。肥胖是高血压的一个重要危险因素,然而这种关系的生理基础尚未阐明。在一项人群调查中,我们研究了RAS与肥胖之间的潜在关系。基于社区抽样,从牙买加金斯敦大都市招募了449名个体。测量了血清血管紧张素转换酶(ACE)和循环血管紧张素原水平,并对相关基因进行分型以检测先前描述的多态性。肥胖个体(体重指数>31)的血清ACE和血管紧张素原水平显著更高,在控制了血压、高血压状态、年龄和性别的多变量分析中,ACE的这种关系依然存在。ACE基因的插入/缺失多态性与ACE水平的变化有关,但与体重指数不一致。血管紧张素原基因在第174和235位导致氨基酸替换的变体既不影响血管紧张素原水平,也不影响肥胖。这些数据表明,肥胖可能会改变ACE和血管紧张素原的水平,并提供了一条肥胖导致血压升高的潜在途径。

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