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.
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