Hilgers K F, Mann J F
Department of Internal Medicine IV, University of Erlangen-Nürnberg, Germany.
Kidney Blood Press Res. 1996;19(5):254-62. doi: 10.1159/000174085.
Angiotensin (Ang) II is generated within the kidney via a complex transcellular pathway. Renin release is not the sole determinant of Ang II levels; the expression of angiotensinogen, Ang-converting enzyme, and angiotensinases may also regulate local Ang II. The Ang II levels in some intrarenal compartments are several orders of magnitude higher than in plasma; plasma measurements may not always predict local Ang II levels. Besides its effects on systemic blood pressure, Ang II modulates glomerular hemodynamics by constricting preferentially the efferent arteriole. The evidence available indicates that both the hemodynamic and nonhemodynamic effects of Ang II are mediated by the type 1 Ang II receptor. Nonhemodynamic effects of Ang II include stimulation of the growth of renal vascular and glomerular cells, increased synthesis of matrix molecules, and possibly a stimulation of monocyte/macrophage infiltration. These effects of the octapeptide may contribute to glomerular sclerosis and interstitial fibrosis. Intervention studies have shown that blockade of Ang II formation by Ang-converting enzyme inhibition reduces proteinuria and delays the progression of renal insufficiency in patients with diabetic and nondiabetic glomerular diseases.
血管紧张素（Ang）II通过复杂的跨细胞途径在肾脏内生成。肾素释放并非Ang II水平的唯一决定因素；血管紧张素原、血管紧张素转换酶和血管紧张素酶的表达也可能调节局部Ang II。一些肾内区域的Ang II水平比血浆中的高出几个数量级；血浆测量结果可能并不总能预测局部Ang II水平。除了对全身血压的影响外，Ang II通过优先收缩出球小动脉来调节肾小球血流动力学。现有证据表明，Ang II的血流动力学和非血流动力学效应均由1型Ang II受体介导。Ang II的非血流动力学效应包括刺激肾血管和肾小球细胞生长、增加基质分子合成以及可能刺激单核细胞/巨噬细胞浸润。这种八肽的这些效应可能导致肾小球硬化和间质纤维化。干预研究表明，通过抑制血管紧张素转换酶来阻断Ang II的形成可减少糖尿病和非糖尿病肾小球疾病患者的蛋白尿，并延缓肾功能不全的进展。
