Mulrow P J
Medical College of Ohio, Department of Medicine, Toledo 43699-0008.
Curr Opin Nephrol Hypertens. 1993 Jan;2(1):41-4. doi: 10.1097/00041552-199301000-00006.
The standard concept of the renin-angiotensin system is that renin is secreted by the juxtaglomerular cells of the kidney into the circulation, where it cleaves angiotensin to release angiotensin I. The angiotensin I is converted to angiotensin II by a converting enzyme located on the plasma membrane of the endothelial cell. The released angiotensin II binds to receptors on target cells to initiate a series of intracellular actions that result in a specific cell function. The kidney was conceived to secrete renin with the circulatory angiotensin II returning to the kidney to alter renal function. It is now clear that all the components of the renin-angiotensin system can be synthesized within the kidney. In fact, angiotensin II is formed in very high concentrations in the renal interstitial space. Local angiotensin II production can have profound influences on renal function, ie, alter glomerular hemodynamics, reduce sodium excretion, and constrict small arterioles. In certain disease states, the local action of angiotensin II may have harmful effects on the kidney, and blockade of the renin-angiotensin system can be beneficial to the kidney.
肾素-血管紧张素系统的标准概念是，肾素由肾脏的球旁细胞分泌进入血液循环，在血液循环中它裂解血管紧张素以释放血管紧张素I。血管紧张素I通过位于内皮细胞质膜上的转换酶转化为血管紧张素II。释放的血管紧张素II与靶细胞上的受体结合，启动一系列细胞内作用，从而导致特定的细胞功能。传统观念认为，肾脏分泌肾素，循环中的血管紧张素II返回肾脏以改变肾功能。现在已经清楚，肾素-血管紧张素系统的所有成分都可以在肾脏内合成。事实上，血管紧张素II在肾间质空间中以非常高的浓度形成。局部血管紧张素II的产生可对肾功能产生深远影响，即改变肾小球血流动力学、减少钠排泄并使小动脉收缩。在某些疾病状态下，血管紧张素II的局部作用可能对肾脏产生有害影响，而阻断肾素-血管紧张素系统可能对肾脏有益。
