VASCULAR ENDOTHELIUM AND DIABETES

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  • FUKAO Mitsuhiro
    Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine
  • TOHSE Noritsugu
    Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine

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  • 血管内皮と糖尿病

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Abstract

Vascular deterioration is one of the complicating features of human and experimental diabetes. Some of the vascular changes in diabetes are related to alterations in endothelial function. In this regard, the vascular responsiveness to endothelium-dependent relaxant agents has been extensively investigated in human and animal models of diabetes. Endothelial cells relax vascular smooth muscle by releasing vasodilating substances, including nitric oxide (NO), PGI2, and endothelium-derived hyperpolarizing factor (EDHF). Impaired endothelium-dependent relaxations have been consistently demonstrated in various vascular beds of diabetic animal models and humans. Several mechanisms of endothelial dysfunction have been reported, impaired signal transduction mechanisms, reduced substrate availability, impaired release of EDRF, increased destruction of EDRF, enhanced release of endothelium-derived constricting factors and decreased sensitivity of the vascular smooth muscle to EDRF. The principal mediators of hyperglycemia-induced endothelial dysfunction may be increased activity of the polyol pathway, activation of protein kinase C, formation of AGEs and oxidative stress. Correction of these pathways, as well as administrations of ACE inhibitors and statins may provide new therapeutic strategies in the treatment of diabetes.

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