Renal angiotensin-converting enzyme and blood pressure control.

Renal angiotensin-converting enzyme and blood pressure control.
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DOI:
10.1097/01.mnh.0000441047.13912.56
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发表时间:
2014-03
影响因子:
3.2
通讯作者:
Gonzalez-Villalobos RA
Gonzalez-Villalobos RA
中科院分区:
医学3区
文献类型:
--
作者:
Bernstein KE;Giani JF;Shen XZ;Gonzalez-Villalobos RA

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本文综述了关于肾血管紧张素转换酶(ACE)及其在血压控制中的作用的新发现。肾素-血管紧张素系统(RAS)的教科书流程图显示,肺内皮是将血管紧张素I转化为血管紧张素II的ACE的主要来源。然而,ACE是由肾脏大量产生的,这就提出了一个重要的问题:肾脏ACE的功能究竟是什么?最近对基因靶向小鼠的研究表明,肾ACE在调节肾脏对实验性高血压的反应中起主导作用。特别是,肾脏ACE和局部生成的血管紧张素II影响几种关键钠转运体的活性,并诱导钠和水潴留,从而导致血压升高。新的实验数据将肾ACE/血管紧张素II通路和钠转运的局部调控作为高血压发展的关键因素联系起来。
This review presents novel findings regarding the renal angiotensin-converting enzyme (ACE) and its role in blood pressure (BP) control. The textbook flow diagram of the renin–angiotensin system (RAS) shows the pulmonary endothelium as the main source of the ACE that converts angiotensin I to angiotensin II. However, ACE is made in large quantities by the kidneys, which raises the important question of what precisely is the function of renal ACE? Recent studies in gene-targeted mice indicates that renal ACE plays a dominant role in regulating the response of the kidney to experimental hypertension. In particular, renal ACE and locally generated angiotensin II affect the activity of several key sodium transporters and the induction of sodium and water retention resulting in the elevation of BP. New experimental data link the renal ACE/angiotensin II pathway and the local regulation of sodium transport as key elements in the development of hypertension.
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