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醛固酮调节的钠转运与血压

Aldosterone-Regulated Sodium Transport and Blood Pressure.

作者信息

Tsilosani Akaki, Gao Chao, Zhang Wenzheng

机构信息

Department of Regenerative & Cancer Cell Biology, Albany Medical College, Albany, NY, United States.

出版信息

Front Physiol. 2022 Feb 7;13:770375. doi: 10.3389/fphys.2022.770375. eCollection 2022.

DOI:10.3389/fphys.2022.770375
PMID:35197862
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8859437/
Abstract

Aldosterone is a major mineralocorticoid steroid hormone secreted by glomerulosa cells in the adrenal cortex. It regulates a variety of physiological responses including those to oxidative stress, inflammation, fluid disruption, and abnormal blood pressure through its actions on various tissues including the kidney, heart, and the central nervous system. Aldosterone synthesis is primarily regulated by angiotensin II, K concentration, and adrenocorticotrophic hormone. Elevated serum aldosterone levels increase blood pressure largely by increasing Na re-absorption in the kidney through regulating transcription and activity of the epithelial sodium channel (ENaC). This review focuses on the signaling pathways involved in aldosterone synthesis and its effects on Na reabsorption through ENaC.

摘要

醛固酮是一种主要的盐皮质类固醇激素,由肾上腺皮质的球状带细胞分泌。它通过作用于包括肾脏、心脏和中枢神经系统在内的各种组织,调节多种生理反应,包括对氧化应激、炎症、液体紊乱和异常血压的反应。醛固酮的合成主要受血管紧张素II、钾浓度和促肾上腺皮质激素调节。血清醛固酮水平升高主要通过调节上皮钠通道(ENaC)的转录和活性,增加肾脏对钠的重吸收,从而升高血压。本综述重点关注醛固酮合成所涉及的信号通路及其对通过ENaC进行钠重吸收的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d5a/8859437/8276e16a6202/fphys-13-770375-g005.jpg
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