Ibrahim H N, Rosenberg M E, Hostetter T H
Department of Medicine-Renal Division, University of Minnesota, Minneapolis 55455, USA.
Semin Nephrol. 1997 Sep;17(5):431-40.
Interruption of the renin-angiotensin-aldosterone system (RAAS) by converting enzyme inhibition or angiotensin II (ANG II) receptor antagonism dramatically reduces injury in the remnant kidney model. Furthermore, converting enzyme inhibition reduces proteinuria and slows the decline in renal function in clinical disease. Hemodynamic actions of ANG II in the kidney in conjunction with a more poorly defined effect of the RAAS on systemic hypertension have been posited as the major mechanisms for maintenance of elevated glomerular pressure. Reductions in glomerular pressure have been attributed, at least in part, to removal of intrarenal effects of ANG II. Growth and fibrotic actions of ANG II may also contribute to progressive renal injury and relief from them reduce injury. The participation of circulating aldosterone in the remnant kidney model has been recently raised. Hyperaldosteronism and adrenal hypertrophy attend the hypertension, proteinuria, and glomerulosclerosis of this model. Although the hemodynamic actions of aldosterone probably account for some of the adverse effects it has in this model, other direct cellular actions may participate in its renal, as well as cardiac and fibrotic consequences. Thus, the RAAS, working through both ANG II and aldosterone, contributes to chronic progressive renal injury.
通过转换酶抑制或血管紧张素II（ANG II）受体拮抗作用来中断肾素-血管紧张素-醛固酮系统（RAAS），可显著减轻残余肾模型中的损伤。此外，转换酶抑制可减少蛋白尿，并减缓临床疾病中肾功能的下降。ANG II在肾脏中的血流动力学作用，以及RAAS对系统性高血压的作用定义更为模糊，这被认为是维持肾小球压力升高的主要机制。肾小球压力的降低至少部分归因于去除了ANG II的肾内作用。ANG II的生长和纤维化作用也可能导致进行性肾损伤，而消除这些作用可减轻损伤。最近有人提出循环醛固酮在残余肾模型中的作用。醛固酮增多症和肾上腺肥大与该模型的高血压、蛋白尿和肾小球硬化有关。虽然醛固酮的血流动力学作用可能解释了它在该模型中的一些不良反应，但其他直接细胞作用可能参与了其对肾脏以及心脏和纤维化的影响。因此，通过ANG II和醛固酮发挥作用的RAAS，会导致慢性进行性肾损伤。
