Khosravi M. نويسنده , Oryan S. نويسنده , Parivar K. نويسنده , Haeri Rohani S.A. نويسنده , Marandi R. نويسنده

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In the present study, it is shown that in vivo oral administration of glibcnclamide (1-10 mg/kglday), an adenosine triphosphate -sensiuvc potassium channel blocker, and yohimbine (1-5 rug/kg/day), an alpha 2-adrenoceptor antagonise potently reduced glycemia in male rats. Diazoxide (1-45 mg/kg/day), a potassium channel opener, and clonidine (0.05-0.5 mg/kg/day), an alpha 2- adrenoceptor agonist, antagonized the effects of glibenclarnidc and yohimbine respectively. Administration of glibenclamide and yohimbine separately decreased the serum glucose levels, so it was expected that coadministration of these two drugs significantly decreased this parameter in fasted animals. It is well known that glibenclamide blocks the potassium channels and it is likely that, yohimbine also blocks these channels, but according to our data, it seems that yohimbine acts via a different binding site to that of glibenc1amide. In this research it is also observed that administration of yohimbine and glibenclamide causes death in rats" it seems that these drugs causes death in the experimental animals by lowering blood glucose level, which were the aim of this study and could be applied as a way to control the environmental health by abolishing rats.

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