自发性高血压大鼠肾血管结构的变化：血管紧张素 II 阻断无影响。

Structural changes in the renal vasculature in the spontaneously hypertensive rat: no effect of angiotensin II blockade.

Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria, Australia.

Clin Exp Pharmacol Physiol. 1996 Sep;23 Suppl 3:S132-5. doi: 10.1111/j.1440-1681.1996.tb03074.x.

Abstract

There is strong evidence for a renal basis to the development of hypertension in the spontaneously hypertensive rat (SHR). Alterations of the SHR renal vasculature, including the glomerulus, may be involved in the initiation and maintenance of hypertension in this animal model. 2. The arterial walls of pre-glomerular vessels of the SHR are hypertrophied compared with WKY vessels. Unlike other vascular beds in the SHR, this hypertrophy is independent of angiotensin II (AngII). 3. Glomerular number and volume are similar between SHR and the normotensive Wistar-Kyoto (WKY) rats. These results provide no support for the theory that a reduced filtration surface area within the kidneys of the SHR contributes to the elevated blood pressure in these animals. 4. Intrarenal hypertrophy may have similar haemodynamic consequences to clipping of the main renal artery, as in Goldblatt hypertension. Further analysis of the role of pre-glomerular arterial hypertrophy is warranted to determine its involvement in the initiation and maintenance of hypertension in the SHR.

摘要

自发性高血压大鼠（SHR）的高血压发展具有很强的肾基础证据。SHR 肾脏血管的改变，包括肾小球，可能参与了该动物模型中高血压的发生和维持。
与 WKY 血管相比，SHR 的肾小球前血管的动脉壁发生了肥大。与 SHR 的其他血管床不同，这种肥大不依赖于血管紧张素 II（AngII）。
SHR 和正常血压的 Wistar-Kyoto（WKY）大鼠的肾小球数量和体积相似。这些结果不支持这样一种理论，即 SHR 肾脏中的滤过表面积减少导致这些动物的血压升高。
肾内肥大可能与 Goldblatt 高血压中的主肾动脉夹闭具有相似的血液动力学后果。进一步分析肾小球前动脉肥大的作用是值得的，以确定其在 SHR 高血压的发生和维持中的参与。