肾素-血管紧张素系统构建在高血压胚胎起源学说中的重要性

查看全文 作　　者：[1]陈友鹏;[2]李健;HOCHER [3]Berthold

机构地区：[1]暨南大学附属第一医院感染科,广东广州510632;[2]暨南大学附属第一医院妇产科,广东广州510632;[3]柏林Charite大学医学院心血管研究中心/药理研究所,德国柏林10115

出　　处：《中国病理生理杂志》索引2010年第26卷第11期,共4页

基　　金：德国柏林Charité大学医学院心血管研究中心/药理学研究所Hocher教授合作交流研究项目 摘　　要：Low birth-weight is now known to be associated with increased rates of hypertension in later life. The renin-angiotensin system (RAS) is mainly involved in the regulation of blood pressure. In animal models, alterations of RAS induced by fetal insults such as gestational protein restriction and placental insufficiency may serve as a potential mechanism critical to the fetal programming of hypertension. Blockade of RAS during the nephrogenic period in rats leads to a marked reduction in nephron numbers as well as low birth-weight. The renal RAS suppression during a critical window of nephrogenesis may be a key component in this programming cascade. This article summarizes the potential mechanisms involved in fetal programming of RAS critical to the development of adult hypertension. 关键词：胎儿肾素-血管紧张素系统低出生体重高血压

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肾素-血管紧张素系统构建在高血压胚胎起源学说中的重要性

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