Role of K+ channels in the vasodilator response to bradykinin in the rat heart

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Abstract
1 The role of K+ channels in the nitric oxide (NO)-independent coronary vasodilator efffect of bradykinin was examined in the Langendorff heart preparation in which nitroarginine was used to inhibit NO synthesis and elevate perfusion pressure; cyclo-oxygenase was inhibited with indomethacin. 2 The K+ channel inhibitors, tetraethylammonium, procaine and charybdotoxin, but not glibenc-lamide, further increased perfusion pressure suggesting a role for K+ channels, other than ATP-sensitive K+ channels, in the regulation of coronary vascular tone under the experimental conditions adopted here. 3 The non-specific K+ channel inhibitors, tetraethylammonium and procaine, reduced vasodilator responses to bradykinin and cromakalim but not those to nitroprusside in the perfused heart treated with nitroarginine and indomethacin. 4 Glibenclamide, an inhibitor of ATP-sensitive K+ channels, reduced vasodilator responses to cromakalim but did not affect those to bradykinin or nitroprusside. 5 Charybdotoxin, an antagonist of Ca2+-activated K+ channels, inhibited responses to bradykinin but did not affect those to cromakalim or nitroprusside. 6 Nifedipine inhibited vasodilator responses to bradykinin and cromakalim without affecting those to nitroprusside. 7 Inhibition of cytochrome P450 with clotrimazole reduced responses to bradykinin but did not modify those to cromakalim or nitroprusside. 8 These results suggest that bradykinin utilizes a Ca2+-activated K+ channel to produce vasodilatation in the rat heart.