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肾素-血管紧张素系统——高血压与肾脏相关考量

Renin-Angiotensin system - considerations for hypertension and kidney.

作者信息

Yim Hyung Eun, Yoo Kee Hwan

机构信息

Department of Pediatrics, Korea University College of Medicine, Seoul, Korea.

出版信息

Electrolyte Blood Press. 2008 Jun;6(1):42-50. doi: 10.5049/EBP.2008.6.1.42. Epub 2008 Jun 30.

Abstract

The kidneys play a fundamental role in the long-term control of arterial pressure by regulating sodium balance and extracellular fluid volume. The renin-angiotensin system (RAS) is at the center of the regulation of hypertension and progressive renal injury. It has gradually become clear that not only systemic RAS, but also intrarenal RAS has specific effects in the pathogenesis and progression of hypertension and renal damage. All of the RAS components are exhibited in the kidney and intrarenal angiotensin II (Ang II) is formed by multiple mechanisms. The demonstration of much enhanced levels of Ang II within specific renal compartments points out selective local regulation of Ang II in the kidney, showing that intrarenal Ang II levels are regulated in a way different from circulating Ang II. The importance of the RAS in involving proper nephrogenesis is also well known, and suppression of the RAS during fetal development may play a key role in mediating the structural and physiological changes observed in models of fetal programming of hypertension.

摘要

肾脏通过调节钠平衡和细胞外液容量,在动脉血压的长期控制中发挥着重要作用。肾素-血管紧张素系统(RAS)是高血压和进行性肾损伤调节的核心。逐渐明确的是,不仅全身RAS,而且肾内RAS在高血压和肾损伤的发病机制及进展中都有特定作用。所有RAS成分都在肾脏中表达,肾内血管紧张素II(Ang II)通过多种机制形成。特定肾区室内Ang II水平显著升高的证据表明,肾脏中Ang II存在选择性局部调节,表明肾内Ang II水平的调节方式与循环中的Ang II不同。RAS在正常肾发生中的重要性也广为人知,胎儿发育期间RAS的抑制可能在介导高血压胎儿编程模型中观察到的结构和生理变化方面起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3446/3894487/585a40706c8e/ebp-6-42-g001.jpg

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