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

David Fulton, John C. McGiff, John Quilley

Research output: Contribution to journalArticle

57 Scopus citations

Abstract

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

Original languageEnglish (US)
Pages (from-to)954-958
Number of pages5
JournalBritish Journal of Pharmacology
Volume113
Issue number3
DOIs
StatePublished - Nov 1994
Externally publishedYes

Keywords

  • K channels
  • Langendorff heart
  • bradykinin‐induced vasodilatation

ASJC Scopus subject areas

  • Pharmacology

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