Effects of sodium tungstate and vanadyl sulphate on the liberation of prostanoids of the mesenteric vascular bed in diabetic rats.

Clin Investig Arterioscler

Cátedra de Anatomía e Histología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Ciudad Autónoma de Buenos Aires, Argentina; Facultad de Medicina, Universidad de Buenos Aires, Instituto de Investigaciones Cardiológicas (ININCA), UBA-CONICET, Ciudad Autónoma de Buenos Aires, Argentina. Electronic address:

Published: March 2019

The loss of the modulator role of the endothelium could be involved in the pathogenesis of diabetic vascular complications. Transition metal compounds, such as tungsten and vanadium, have been proposed as possible agents in the treatment of diabetes by simulating the effects of insulin. The mesenteric vascular bed intervenes in vascular resistance and is a source of vasoactive compounds, such as prostanoids. The aim of this work was to study the effects of sodium tungstate and vanadyl sulphate treatments on the metabolic parameters and the release of prostanoids of the mesenteric vascular bed in an experimental model of Streptozotocin-induced diabetes. In diabetic rats, a significant increase was observed in plasma levels of glucose, triglycerides and total cholesterol. On the other hand, there was a significant reduction in the release of vasodilator prostanoids, such as prostacyclin and prostaglandin E and vasoconstrictor thromboxane A through the mesenteric vascular bed. Both sodium tungstate and vanadyl sulphate normalised glycaemia, triglyceridaemia and cholesterolaemia in rats diabetics. On the other hand, only treatment with sodium tungstate reversed the reduction in the release of vasodilator prostanoids, improving in diabetic animals the prostacyclin/thromboxane ratio, an indicator of vascular dysfunction. In conclusion, unlike vanadyl sulphate, sodium tungstate is shown to be more effective in controlling metabolic changes and the production of vasodilator prostanoids observed in experimental diabetes induced by streptozotocin.

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Source
http://dx.doi.org/10.1016/j.arteri.2018.04.001DOI Listing

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