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Cromakalim, pinacidil and nitroprusside provoked concentration-dependent relaxations of K⁺-depolarized rat aortae. Glibenclamide, tolbutamide and to a lesser extent tetraethylammonium antagonized the vasorelaxant action of cromakalim and pinacidil. Cromakalim, pinacidil but not nitroprusside elicited a marked increase in ⁸⁶Rb outflow from preloaded and perifused aortic rings. These increases in ⁸⁶Rb outflow were inhibited in a concentration-dependent manner by glibenclamide and tetraethylammonium. Our data extend previous observations indicating the involvement of K⁺ channels in the vasorelaxant properties of cromakalim and pinacidil. Moreover, the present findings suggest that both compounds could interfere with a vascular type of ATP-sensitive K⁺ channels.

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