Ibrahim H N, Rosenberg M E, Greene E L, Kren S, Hostetter T H
Department of Medicine, University of Minnesota, Minneapolis, USA.
Kidney Int Suppl. 1997 Dec;63:S115-9.
There is compelling evidence supporting the renin-angiotensin-aldosterone system contribution in experimental and human renal disease. Interruption of this system by converting enzyme inhibition or angiotensin II receptor antagonism reduces injury. Angiotensin II contributes to the progression of renal disease through its direct vascular effects and proliferative properties. The mediators of angiotensin II induced renal injury are many and include TGF-beta, PDGF, bFGF, and endothelin. Though the mechanisms involved in its contribution to progressive renal disease are not well delineated, aldosterone seems to be an overlooked contributor to the progression of kidney disease and its effects may also depend on both its hemodynamic and more direct cellular actions.
有令人信服的证据支持肾素 - 血管紧张素 - 醛固酮系统在实验性和人类肾脏疾病中的作用。通过抑制转换酶或拮抗血管紧张素II受体来中断该系统可减轻损伤。血管紧张素II通过其直接的血管效应和增殖特性促进肾脏疾病的进展。血管紧张素II诱导肾损伤的介质众多，包括转化生长因子 - β、血小板衍生生长因子、碱性成纤维细胞生长因子和内皮素。尽管其在进行性肾脏疾病中的作用机制尚未完全阐明，但醛固酮似乎是肾脏疾病进展中一个被忽视的因素，其作用可能还取决于其血流动力学和更直接的细胞作用。
