Department of Cardiology & Kolling Institute of Medical Research, Royal North Shore Hospital & University of Sydney, Pacific Highway, St. Leonards, Sydney, NSW, Australia, 2065.
Curr Hypertens Rep. 2012 Apr;14(2):125-9. doi: 10.1007/s11906-012-0256-9.
Numerous studies have now shown that sustained elevation of aldosterone levels induces cardiovascular damage independent from its effects on regulation of renal sodium and blood pressure. Increased aldosterone and cortisol levels in patients with heart failure independently predict the risk of mortality. Over the past decade, there has been increased interest in identifying the role of the receptor for aldosterone, the mineralocorticoid receptor (MR), following the results from the large clinical heart failure trials that showed low doses of MR antagonists reduced morbidity and mortality in heart failure and myocardial infarction, even though plasma levels of aldosterone were in the physiologic range. The mechanism for this cardioprotective action remains to be defined, although changes in the redox state have been shown to play a key role in MR-mediated cardiac damage. This review will highlight some of these studies and provide an update on the action of aldosterone in heart disease.
大量研究表明，醛固酮水平持续升高会导致心血管损伤，而与调节肾脏钠和血压的作用无关。心力衰竭患者的醛固酮和皮质醇水平升高可独立预测死亡风险。在过去十年中，人们越来越关注醛固酮受体，即盐皮质激素受体 (MR) 的作用，这是因为大型心力衰竭临床试验的结果表明，低剂量的 MR 拮抗剂可降低心力衰竭和心肌梗死的发病率和死亡率，尽管醛固酮的血浆水平处于生理范围内。这种心脏保护作用的机制仍有待确定，尽管氧化还原状态的变化已被证明在 MR 介导的心脏损伤中发挥关键作用。本文将重点介绍其中的一些研究，并更新醛固酮在心脏病中的作用。
