Dargie H J, Byrne J
Glasgow Clinical Research Initiative in Heart Failure, University of Glasgow, UK.
J Cardiovasc Risk. 1995 Oct;2(5):389-95. doi: 10.1177/174182679500200502.
Our understanding of the renin-angiotensin-aldosterone system (RAAS) has advanced considerably in recent years. The RAAS plays a central role in the control of salt and water balance, and in the regulation of blood pressure and cardiovascular homeostasis. The haemodynamic changes in the period after myocardial infarction stimulate intense activation of both the circulating and the local RAAS. This acts through its end-products, angiotensin II and aldosterone, to promote sodium and fluid retention, and to increase cardiac contractility and systemic vascular tone. There is increasing evidence that, in the long term, this apparently adaptive response may be harmful, and might contribute to the development of some of the complications seen after infarction. Angiotensin II is capable of inducing coronary as well as systemic vasoconstriction, and may therefore prolong the duration of ischaemia. The response of the RAAS after infarction can be modified pharmacologically. Angiotensin converting enzyme (ACE) inhibitor drugs are already the mainstay of treatment in heart failure, and have now been shown to have a crucial role in the prevention of ventricular remodelling after myocardial infarction. Although the precise mechanism of this benefit is unclear, it provides further incentives to develop more effective strategies capable of suppressing neurohumoral activity following infarction.
近年来，我们对肾素-血管紧张素-醛固酮系统（RAAS）的认识有了很大进展。RAAS在控制盐和水平衡以及调节血压和心血管稳态方面发挥着核心作用。心肌梗死后一段时间内的血流动力学变化会刺激循环和局部RAAS的强烈激活。这通过其终产物血管紧张素II和醛固酮起作用，促进钠和液体潴留，并增加心脏收缩力和全身血管张力。越来越多的证据表明，从长期来看，这种明显的适应性反应可能是有害的，并且可能导致梗死后期出现的一些并发症。血管紧张素II能够诱导冠状动脉以及全身血管收缩，因此可能会延长缺血时间。梗死后RAAS的反应可以通过药物进行调节。血管紧张素转换酶（ACE）抑制剂药物已经是心力衰竭治疗的主要药物，现在已被证明在预防心肌梗死后心室重构方面具有关键作用。尽管这种益处的确切机制尚不清楚，但它进一步促使人们开发更有效的策略来抑制梗死后的神经体液活性。
