par Antoine, Marie-Hélène 
;Berkenboom, Guy ;Fang, Z. Y.;Fontaine, J;Herchuelz, André ;Lebrun, Philippe
Référence European journal of pharmacology, 216, 2, page (299-306)
Publication Publié, 1992-06
;Berkenboom, Guy ;Fang, Z. Y.;Fontaine, J;Herchuelz, André ;Lebrun, Philippe Référence European journal of pharmacology, 216, 2, page (299-306)
Publication Publié, 1992-06
Article révisé par les pairs
| Résumé : | Diazoxide provoked concentration-dependent and endothelium-independent relaxations of the mechanical responses evoked by low concentrations of KCl. Glibenclamide, tolbutamide and tetraethylammonium shifted the concentration-response curve for diazoxide to the right. The drug also caused a dose-dependent stimulation of 86Rb outflow which was inhibited by glibenclamide and tolbutamide. Diazoxide (10(-4) and 10(-3) M) inhibited the contractions elicited by 10(-1) M K+ and provoked a concentration-dependent reduction in the contractile responses to Ca2+. Diazoxide also reduced the KCl (8 x 10(-2) M)-induced increase in 45Ca outflow. These data indicate that the vasorelaxant properties of diazoxide are probably related to an inhibition of Ca2+ entry into smooth muscle cells. The reduction in Ca2+ entry appears to result from K+ channel activation. At high concentrations, diazoxide also exhibited antagonistic actions on voltage-sensitive Ca2+ channels. |
