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

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

Biological and Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

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 language	English
Journal	British Journal of Pharmacology
Publication status	Published - 1 Oct 2002

Keywords

endothelium
Endothelium-derived hyperpolarizing factor
guanylyl cyclase
nitric oxide

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

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.",

keywords = "endothelium, Endothelium-derived hyperpolarizing factor, guanylyl cyclase, nitric oxide",

author = "A. Tracey and D. Bunton and J. Irvine and Allan MacDonald and Shaw, {Angus M.}",

note = "Originally published in: British Journal of Pharmacology (2002), 137 (4), pp.538-544.",

year = "2002",

month = oct,

day = "1",

language = "English",

journal = "British Journal of Pharmacology",

issn = "0007-1188",

publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Relaxation to bradykinin in bovine pulmonary supernumerary arteries can be mediated by both a nitric oxide-dependent and -independent mechanism

AU - Tracey, A.

AU - Bunton, D.

AU - Irvine, J.

AU - MacDonald, Allan

AU - Shaw, Angus M.

N1 - Originally published in: British Journal of Pharmacology (2002), 137 (4), pp.538-544.

PY - 2002/10/1

Y1 - 2002/10/1

N2 - 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.

AB - 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.

KW - endothelium

KW - Endothelium-derived hyperpolarizing factor

KW - guanylyl cyclase

KW - nitric oxide

M3 - Article

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

ER -