Division of Pharmacology and Vascular Medicine, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands.
Nephrol Dial Transplant. 2013 Dec;28(12):2977-82. doi: 10.1093/ndt/gft333. Epub 2013 Jul 30.
A large body of evidence supports the presence of local production of angiotensins in the kidney. It is widely believed that renin-angiotensin system (RAS) blockers, through interference with such production and/or the local effects of angiotensin (Ang) II, exert protective renal effects. Yet, whether such production affects blood pressure independently from the circulating RAS is still a matter of debate. To investigate this, a recent study by Gonzalez-Villalobos et al. (J Clin Invest 2013; 123: 2011-2023) has studied the consequences of infusing Ang II or the nitric oxide synthase inhibitor l-NAME in mice lacking renal angiotensin-converting enzyme (ACE). They observed blunted blood pressure and renal responses in the renal ACE knockout mice versus wild-type controls. This review discusses to what degree these findings can be considered as unequivocal evidence for ACE-mediated Ang II formation in the kidney as an independent determinant of hypertension.
大量证据表明肾内局部可生成血管紧张素。人们普遍认为肾素-血管紧张素系统（RAS）阻滞剂通过干扰这种生成和/或血管紧张素（Ang）II 的局部作用发挥肾脏保护作用。然而，这种生成是否会独立于循环 RAS 对血压产生影响仍存在争议。为了研究这一问题，Gonzalez-Villalobos 等人（J Clin Invest 2013; 123: 2011-2023）最近在缺乏肾血管紧张素转换酶（ACE）的小鼠中进行了输注 Ang II 或一氧化氮合酶抑制剂 l-NAME 的研究。他们观察到肾 ACE 敲除小鼠与野生型对照相比，血压和肾脏反应减弱。这篇综述讨论了这些发现在多大程度上可以被认为是 ACE 介导的肾内 Ang II 形成作为高血压独立决定因素的确凿证据。
