Stoian Marilena, Radulian Gabriela, Chiţac Delia, Simion E, Stoica V
I. Cantacuzino Hospital, Clinic of Internal Medicine, Bucharest, Romania.
Rom J Intern Med. 2007;45(2):215-8.
The role of the renin angiotensin system (RAS) in hypertension and end organ damage has long been recognized. Angiotensin 1 converting enzyme inhibitors (ACEI) are superior to other antihypertensive agents in protecting the kidney against progressive deterioration, even in normotensive persons. Like ACEI, angiotensin II type 1 receptor antagonists (AT1RA) ameliorate or even reverse glomerulosclerosis in rat animal models. These findings suggest that Angiotensin II (Ang II) has nonhemodynamic effects in progressive renal disease. The RAS is now recognized to be linked to induction of plasminogen activator-inhibitor-1 (PAI-1), possibly via the AT4 receptor, thus promoting both thrombosis and fibrosis. Interactions of the RAS with aldosterone and bradykinin may have an impact on both blood pressure and tissue injury. 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 various actions. This article explores the interaction of the renin angiotensin aldosterone system with PAI-1, and the potential significance of these interactions in the pathogenesis of progressive renal disease and remodeling of renal sclerosis.
肾素血管紧张素系统（RAS）在高血压和终末器官损害中的作用早已得到认可。血管紧张素1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，即使在血压正常的人群中也是如此。与ACEI一样，血管紧张素II 1型受体拮抗剂（AT1RA）在大鼠动物模型中可改善甚至逆转肾小球硬化。这些发现表明，血管紧张素II（Ang II）在进行性肾脏疾病中具有非血流动力学效应。现在认为RAS与纤溶酶原激活物抑制剂-1（PAI-1）的诱导有关，可能是通过AT4受体，从而促进血栓形成和纤维化。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。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各种作用在调节肾功能和结构中所起的核心作用。本文探讨了肾素血管紧张素醛固酮系统与PAI-1的相互作用，以及这些相互作用在进行性肾脏疾病发病机制和肾硬化重塑中的潜在意义。
