TY - JOUR
T1 - Role of K+ channels in the vasodilator response to bradykinin in the rat heart
AU - Fulton, David
AU - McGiff, John C.
AU - Quilley, John
PY - 1994/11
Y1 - 1994/11
N2 - 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. 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. 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. Glibenclamide, an inhibitor of ATP‐sensitive K+ channels, reduced vasodilator responses to cromakalim but did not affect those to bradykinin or nitroprusside. Charybdotoxin, an antagonist of Ca2+‐activated K+ channels, inhibited responses to bradykinin but did not affect those to cromakalim or nitroprusside. Nifedipine inhibited vasodilator responses to bradykinin and cromakalim without affecting those to nitroprusside. Inhibition of cytochrome P450 with clotrimazole reduced responses to bradykinin but did not modify those to cromakalim or nitroprusside. These results suggest that bradykinin utilizes a Ca2+‐activated K+ channel to produce vasodilatation in the rat heart. 1994 British Pharmacological Society
AB - 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. 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. 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. Glibenclamide, an inhibitor of ATP‐sensitive K+ channels, reduced vasodilator responses to cromakalim but did not affect those to bradykinin or nitroprusside. Charybdotoxin, an antagonist of Ca2+‐activated K+ channels, inhibited responses to bradykinin but did not affect those to cromakalim or nitroprusside. Nifedipine inhibited vasodilator responses to bradykinin and cromakalim without affecting those to nitroprusside. Inhibition of cytochrome P450 with clotrimazole reduced responses to bradykinin but did not modify those to cromakalim or nitroprusside. These results suggest that bradykinin utilizes a Ca2+‐activated K+ channel to produce vasodilatation in the rat heart. 1994 British Pharmacological Society
KW - K channels
KW - Langendorff heart
KW - bradykinin‐induced vasodilatation
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U2 - 10.1111/j.1476-5381.1994.tb17085.x
DO - 10.1111/j.1476-5381.1994.tb17085.x
M3 - Article
C2 - 7858891
AN - SCOPUS:0027960639
SN - 0007-1188
VL - 113
SP - 954
EP - 958
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
IS - 3
ER -