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首页> 外文期刊>Current hypertension reports. >The kidneys and aldosterone/mineralocorticoid receptor system in salt-sensitive hypertension.
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The kidneys and aldosterone/mineralocorticoid receptor system in salt-sensitive hypertension.

机译:盐敏感性高血压患者的肾脏和醛固酮/盐皮质激素受体系统。

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摘要

Strong evidence supports the ability of the aldosterone/mineralocorticoid receptor (MR) system to dominate long-term blood pressure control. It is also increasingly recognized as an important mediator of cardiovascular and renal diseases, particularly in the presence of excessive salt intake. In a subgroup of individuals with metabolic syndrome, adipocyte-derived aldosterone-releasing factors cause inappropriate secretion of aldosterone in the adrenal glands during salt loading, resulting in the development of salt-induced hypertension and cardiac and renal damage. On the other hand, emerging data reveal that aldosterone is not a sole regulator of MR activity. We have identified the signaling crosstalk between MR and small GTPase Rac1 as a novel pathway to facilitate MR signaling. Such a local control system for MR can also be relevant to the pathogenesis of salt-sensitive hypertension, and future studies will clarify the detailed mechanism for the intricate regulation of the aldosterone/MR cascade.
机译:有力的证据支持醛固酮/盐皮质激素受体(MR)系统主导长期血压控制的能力。它也日益被认为是心血管和肾脏疾病的重要介质,尤其是在盐摄入量过多的情况下。在一组患有代谢综合征的人群中,源自脂肪细胞的醛固酮释放因子会在盐负荷期间导致肾上腺中醛固酮的分泌不当,从而导致盐诱导的高血压以及心脏和肾脏的损害。另一方面,新出现的数据表明,醛固酮不是MR活性的唯一调节剂。我们已经确定了MR和小的GTPase Rac1之间的信号传递串扰是促进MR信号传递的新途径。这种用于MR的局部控制系统也可能与盐敏感性高血压的发病机理有关,未来的研究将阐明复杂调节醛固酮/ MR级联反应的详细机制。

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