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醛固酮会损害血管内皮细胞功能。

Aldosterone impairs vascular endothelial cell function.

作者信息

Hashikabe Yuko, Suzuki Kunihiro, Jojima Teruo, Uchida Kohsuke, Hattori Yoshiyuki

机构信息

Department of Endocrinology and Metabolism, Dokkyo University School of Medicine, Mibu, Tochigi, Japan.

出版信息

J Cardiovasc Pharmacol. 2006 Apr;47(4):609-13. doi: 10.1097/01.fjc.0000211738.63207.c3.

Abstract

Aldosterone is a mineralocorticoid hormone that plays an important role in regulating electrolyte balance and blood pressure and also participates in endothelial dysfunction. We evaluated the direct effect of aldosterone on human umbilical vein cells (HUVEC). Levels of eNOS phosphorylation by vascular endothelial growth factor were diminished, and the amount of NO produced in response to vascular endothelial growth factor measured as NO2+NO3 was significantly decreased in cells previously incubated with aldosterone. Incubation with aldosterone for 24 h dose-dependently increased Nox4 mRNA expression in HUVEC. Although NF-kappaB was not apparently activated by aldosterone, mRNA levels of vascular cell adhesion molecule-1, E-selectin, monocyte chemotactic protein-1, and intercellular adhesion molecule-1 in HUVEC were significantly increased after incubation with aldosterone. Thus, aldosterone directly causes the dysregulation of endothelial cell function, which may be partly responsible for high blood pressure and atherosclerosis.

摘要

醛固酮是一种盐皮质激素,在调节电解质平衡和血压方面发挥重要作用,还参与内皮功能障碍。我们评估了醛固酮对人脐静脉细胞(HUVEC)的直接作用。血管内皮生长因子引起的内皮型一氧化氮合酶(eNOS)磷酸化水平降低,并且在先前用醛固酮孵育的细胞中,对血管内皮生长因子作出反应而产生的以NO2+NO3衡量的一氧化氮(NO)量显著减少。用醛固酮孵育24小时剂量依赖性地增加了HUVEC中Nox4 mRNA的表达。尽管醛固酮未明显激活核因子κB(NF-κB),但在HUVEC中用醛固酮孵育后,血管细胞黏附分子-1、E-选择素、单核细胞趋化蛋白-1和细胞间黏附分子-1的mRNA水平显著增加。因此,醛固酮直接导致内皮细胞功能失调,这可能部分导致高血压和动脉粥样硬化。

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