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钒与心血管功能

Vanadium and the cardiovascular functions.

作者信息

Coderre Lise, Srivastava Ashok K

机构信息

Research Center, Centre hospitalier de l'Université de Montréal, Hôtel-Dieu, Department of Medicine, Université de Montréal, QC, Canada.

出版信息

Can J Physiol Pharmacol. 2004 Oct;82(10):833-9. doi: 10.1139/y04-089.

Abstract

Inorganic and organic compounds of vanadium have been shown to exhibit a large range of insulinomimetic effects in the cardiovascular system, including stimulation of glucose transporter 4 (GLUT-4) translocation and glucose transport in adult cardiomyocytes. Furthermore, administration of vanadium compounds improves cardiac performance and smooth muscle contractility, and modulates blood pressure in various models of hypertension and insulin resistance. Vanadium compounds are potent inhibitors of protein tyrosine phosphatases. As a result, they promote an increase in protein tyrosine phosphorylation of several key components of the insulin signaling pathway, leading to the upregulation of phosphatidylinositol 3-kinase and protein kinase B, two enzymes involved in mediating GLUT-4 trans location and glucose transport. In addition, vanadium has also been shown to activate p38 mitogen-activated protein kinase and increase Ca2+ levels in several cell types. The ability of vanadium compounds to activate these signaling events may be responsible for their ability to modulate cardiovascular functions.

摘要

钒的无机和有机化合物已被证明在心血管系统中表现出广泛的类胰岛素效应,包括刺激成年心肌细胞中的葡萄糖转运蛋白4(GLUT-4)易位和葡萄糖转运。此外,在各种高血压和胰岛素抵抗模型中,施用钒化合物可改善心脏功能和平滑肌收缩力,并调节血压。钒化合物是蛋白质酪氨酸磷酸酶的有效抑制剂。因此,它们促进胰岛素信号通路几个关键成分的蛋白质酪氨酸磷酸化增加,导致磷脂酰肌醇3激酶和蛋白激酶B上调,这两种酶参与介导GLUT-4易位和葡萄糖转运。此外,钒还被证明可激活p38丝裂原活化蛋白激酶并增加几种细胞类型中的Ca2+水平。钒化合物激活这些信号事件的能力可能是其调节心血管功能的原因。

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