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Aldosterone as a Cardiovascular Risk Hormone

机译:醛固酮作为心血管危险激素

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The pathophysiological role of aldosterone in the development of cardiovascular disease has long been considered to be due its potent volume expansion/hypertensive effect mainly via mineralocorticoid receptor (MR) expressed in renal tubular epithelial cells. However, recent accumulating lines of evidence from clinical and experimental studies have suggested that direct cardiovascular effect of aldosterone contributes to the development of cardiovascular injury via MRs in non-epithelial tissue. A series of recent clinical studies have revealed that patients with primary aldosteronism have higher incidence of cardiovascular and renal complications than those with essential hypertension, and that aldosterone antagonism has cardiovascular protective effect in patients with heart failure independent from blood pressure. Numerous experimental studies have shown that both inflammation and oxidative stress play an initial and key role in the development of aldosterone-induced cardiovascular injury via non-epithelial MR activation. In this review, we discuss recent research progress in aldosterone and MR effects, with special emphasis on the pathophysiological role of aldosterone in cardiovascular diseases and the possible molecular mechanism(s) of cardiovascular injury by non-epithelial MR activation.
机译:长期以来,醛固酮在心血管疾病发展中的病理生理作用一直被认为是由于其有效的体积膨胀/高血压作用,主要是通过肾小管上皮细胞中表达的盐皮质激素受体(MR)引起的。然而,最近来自临床和实验研究的越来越多的证据表明,醛固酮的直接心血管作用通过非上皮组织中的MR促进了心血管损伤的发展。最近的一系列临床研究表明,原发性醛固酮增多症患者比原发性高血压患者的心血管和肾脏并发症发生率更高,醛固酮拮抗作用对独立于血压的心力衰竭患者具有心血管保护作用。大量实验研究表明,炎症和氧化应激在醛固酮诱导的非上皮MR激活心血管损伤的发展中起着重要的关键作用。在这篇综述中,我们讨论了醛固酮和MR效应的最新研究进展,特别着重于醛固酮在心血管疾病中的病理生理作用,以及非上皮MR激活引起的心血管损伤的可能分子机制。

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