Relaxation to bradykinin in bovine pulmonary supernumerary arteries can be mediated by both a nitric oxide-dependent and -independent mechanism

A. Tracey, D. Bunton, J. Irvine, Allan MacDonald, Angus M. Shaw

Research output: Contribution to journalArticle

Abstract

The aim of the present study was to determine the relative contribution of prostanoids, nitric oxide and K+ channels in the bradykinin-induced relaxation of bovine pulmonary supernumerary arteries. These studies suggest that in bovine pulmonary supernumerary arteries bradykinin can stimulate the formation of nitric oxide and activate an EDHF-like mechanism and that either of these pathways alone can mediate the bradykinin-induced relaxation. In addition nitric oxide, acting through guanylyl cyclase, can activate an apamin/charbydotoxin-sensitive K+ channel in this tissue.

Original languageEnglish
JournalBritish Journal of Pharmacology
Publication statusPublished - 1 Oct 2002

Keywords

  • endothelium
  • Endothelium-derived hyperpolarizing factor
  • guanylyl cyclase
  • nitric oxide

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