醛固酮在心血管系统中的新作用作为治疗干预的潜在靶点

Title:New Sides of Aldosterone Action in Cardiovascular System as Potential Targets for Therapeutic Intervention

Volume: 19 Issue: 16

关键词: 醛固酮、基因组、非基因组、矿物皮质激素受体、糖皮质激素受体、血管紧张素Ⅱ受体1型、G蛋白偶联雌激素受体。

摘要: Aldosterone, the main mineralocorticoid hormone, plays a crucial role in the regulation of electrolyte homeostasis and blood pressure. Although this role is undoubtedly important, it is not a hormonal action that attracts the most attention. Aldosterone seems to be very important as a local messenger in the pathology of cardiovascular diseases (CVD). In the last few years, the attention was focused on the correlation between raised aldosterone level and increased risk of cardiovascular events. It has been demonstrated that aldosterone contributes to fibrosis, inflammation, endothelial dysfunction, fibrinolytic disorders, and oxidative stress leading to CVD development and progression. It used to be thought that the effects of aldosterone are mediated via classic nuclear receptors – mineralocorticoid receptors (MRs). Now we know that the mechanism of aldosterone action in the cardiovascular system (CVS) is much more complex since experimental and clinical studies indicate that MR blockade may be not sufficient to abolish aldosterone-induced harmful effects in CVS. Thus, the involvement of some other than MR, receptors, and factors is suggested. Moreover, in addition to the generally known genomic action of aldosterone, which involves MR activation, the nongenomic pathways are postulated in the mode of hormone action. More and more attention is focused on the membrane-coupled receptors, which mediate the rapid effects of aldosterone and have been already confirmed in different cells and tissues of CVS. Therefore, this brief review summarizes recent findings about new sides of aldosterone action in CVS that could be potential targets for therapeutic intervention.

Cite this article as:

New Sides of Aldosterone Action in Cardiovascular System as Potential Targets for Therapeutic Intervention, Current Drug Targets 2018; 19 (16) . https://dx.doi.org/10.2174/1389450119666180326125926