Gilbert R E, Krum H, Wilkinson-Berka J, Kelly D J
University of Melbourne, Department of Medicine (St. Vincent's Hospital), Victoria, Australia.
Diabet Med. 2003 Aug;20(8):607-21. doi: 10.1046/j.1464-5491.2003.00979.x.
The relationship between the renin-angiotensin system (RAS) and the progression of diabetic renal disease has been a major focus of investigation over the past 20 years. More recently, experimental and clinical studies have also suggested that the RAS may have a pathogenetic role at other sites of micro- and macrovascular injury in diabetes. Complementing major advances into the understanding of the local, as distinct from the systemic RAS, a number of large clinical trials have examined whether blockade of the RAS might provide protection from the long-term complications of diabetes, beyond that due to blood pressure reduction alone. While some controversy remains, these studies have, in general, suggested that angiotensin converting enzyme (ACE) inhibition and more recently, angiotensin receptor blockade reduce the development and progression of diabetic nephropathy, cardiovascular disease and possibly retinopathy. This review will focus on recent developments in our understanding of the tissue-based RAS and its role in end-organ injury in diabetes, the results of recent clinical trials and newer strategies for the pharmacological manipulation of the RAS.
在过去20年里，肾素-血管紧张素系统（RAS）与糖尿病肾病进展之间的关系一直是研究的主要焦点。最近，实验和临床研究还表明，RAS可能在糖尿病微血管和大血管损伤的其他部位具有致病作用。在对局部RAS（有别于全身RAS）的理解取得重大进展的同时，一些大型临床试验研究了RAS阻断是否可能为糖尿病长期并发症提供保护，而不仅仅是通过降低血压来实现。尽管仍存在一些争议，但总体而言，这些研究表明，血管紧张素转换酶（ACE）抑制以及最近的血管紧张素受体阻断可减少糖尿病肾病、心血管疾病以及可能的视网膜病变的发生和进展。本综述将聚焦于我们对基于组织的RAS及其在糖尿病终末器官损伤中的作用的最新认识进展、近期临床试验结果以及RAS药理调控的新策略。
