Clinical perspectives and fundamental aspects of local cardiovascular and renal Renin-Angiotensin systems.
Clinical perspectives and fundamental aspects of local cardiovascular and renal Renin-Angiotensin systems.
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DOI：
10.3389/fendo.2014.00016
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发表时间：
2014
影响因子：
5.2
通讯作者：
Frohlich ED
中科院分区：
文献类型：
--
作者：
De Mello WC;Frohlich ED
器官特异性心血管肾素-血管紧张素系统(RAS)的潜在作用的证据已经在实验和临床上被证明与某些心血管和肾脏疾病有关。这些发现得到了以下研究的支持：缺血性心脏病、心肌梗死、心力衰竭期间的药物抑制；与左心室缺血、心肌纤维化和左心室肥厚相关的高血压；与长期饮食盐过量有关的靶器官的结构和功能变化；以及与终末期肾脏疾病相关的肾内血管疾病。此外，由这些病理条件引起的严重的结构和功能变化可以通过产生RAS抑制的药物来预防和逆转(即使不一定与动脉压的变化相一致)。在这篇综述中，我们讨论了与局部RAS的激活或抑制有关的特定的基础和临床方面和机制，以及它们对心血管和肾脏疾病的影响。讨论了血管紧张素在心脏和肾脏功能中的作用，包括RAS组分在心脏和肾脏的表达，以及血管紧张素转换酶2在人类血管紧张素肽代谢中的有争议的作用。
Evidence for the potential role of organ specific cardiovascular renin–angiotensin systems (RAS) has been demonstrated experimentally and clinically with respect to certain cardiovascular and renal diseases. These findings have been supported by studies involving pharmacological inhibition during ischemic heart disease, myocardial infarction, cardiac failure; hypertension associated with left ventricular ischemia, myocardial fibrosis and left ventricular hypertrophy; structural and functional changes of the target organs associated with prolonged dietary salt excess; and intrarenal vascular disease associated with end-stage renal disease. Moreover, the severe structural and functional changes induced by these pathological conditions can be prevented and reversed by agents producing RAS inhibition (even when not necessarily coincident with alterations in arterial pressure). In this review, we discuss specific fundamental and clinical aspects and mechanisms related to the activation or inhibition of local RAS and their implications for cardiovascular and renal diseases. Fundamental aspects involving the role of angiotensins on cardiac and renal functions including the expression of RAS components in the heart and kidney and the controversial role of angiotensin-converting enzyme 2 on angiotensin peptide metabolism in humans, were discussed.
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影响因子：
5.2
作者：
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通讯作者：
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通讯作者：
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