Ma L, Fogo A B
Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Semin Nephrol. 2001 Nov;21(6):544-53. doi: 10.1053/snep.2001.26793.
The components of the renin-angiotensin system (RAS) in progressive renal disease have been extensively investigated, indicating multiple actions beyond hemodynamic and salt/water homeostasis. Studies in various human diseases and in animal models have shown that angiotensin (Ang) I-converting enzyme inhibitors (ACEI) are superior to other antihypertensive agents in protecting the kidney against progressive deterioration, even in conditions without systemic hypertension. These findings suggest that Ang II has nonhemodynamic effects in progressive renal disease. Interactions of the RAS with aldosterone and bradykinin may have impact on both blood pressure and tissue injury. The RAS is now recognized to be linked to induction of plasminogen activator inhibitor-1 (PAI-1) likely via both the type 1 (AT1) and type 4 (AT4) receptors, thus, promoting both thrombosis and fibrosis. A role of angiotensin in the regulation of immune injury and inflammation has also been identified. Polymorphisms of genes relevant to the RAS appear to affect the risk and course of cardiovascular and renal diseases and response to treatment. The beneficial effect on renal fibrosis of inhibiting the RAS likely reflects the central role that angiotensin has in regulating renal function and structure by its multifaceted actions. This article will focus on the role of the RAS in glomerular injury.
肾素-血管紧张素系统（RAS）在进行性肾病中的组成部分已得到广泛研究，表明其作用不仅限于血流动力学和盐/水平衡。对各种人类疾病和动物模型的研究表明，血管紧张素（Ang）I转换酶抑制剂（ACEI）在保护肾脏免受进行性损害方面优于其他抗高血压药物，即使在没有系统性高血压的情况下也是如此。这些发现表明，Ang II在进行性肾病中具有非血流动力学效应。RAS与醛固酮和缓激肽的相互作用可能对血压和组织损伤都有影响。现在认为RAS可能通过1型（AT1）和4型（AT4）受体与纤溶酶原激活物抑制剂-1（PAI-1）的诱导有关，从而促进血栓形成和纤维化。血管紧张素在免疫损伤和炎症调节中的作用也已得到确认。与RAS相关的基因多态性似乎会影响心血管和肾脏疾病的风险、病程及对治疗的反应。抑制RAS对肾纤维化的有益作用可能反映了血管紧张素通过其多方面作用在调节肾功能和结构中所起的核心作用。本文将重点探讨RAS在肾小球损伤中的作用。
