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Article: Adrenergic and cholinergic responsiveness of isolated canine bronchial arteries

TitleAdrenergic and cholinergic responsiveness of isolated canine bronchial arteries
Authors
Issue Date1990
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1990, v. 259 n. 1 28-1, p. H156-H161 How to Cite?
AbstractThe purpose of this study was to characterize the adrenergic and cholinergic responsiveness of isolated rings of canine bronchial arteries. Electrical stimulation of the vessels produced frequency-dependent contractions that were inhibited by phenoxybenzamine, tetrodotoxin, and phentolamine but not by atropine. Norepinephrine caused concentration-dependent contractions of the rings; the concentration-response curve to norepinephrine was shifted to the right by phentolamine and prazosin, whereas rauwolscine had no effect. Isoproterenol, norepinephrine, tyramine, and electrical stimulation (in the presence of phentolamine) failed to elicit relaxation in rings contracted with prostaglandin F(2α). Contracted rings relaxed to acetylcholine in an endothelium- and concentration-dependent manner. At concentrations up to 10-4 M, acetylcholine did not evoke contractions in these tissues. Endothelium-dependent relaxation to acetylcholine was inhibited by atropine and 4-diphenyl-acetoxy-N-methyl piperidine methiodine but not by pirenzepine. These results suggest that α1-adrenoceptors mediate contraction to norepinephrine, and M3-muscarinic receptors mediate endothelium-dependent relaxation to acetylcholine in the canine bronchial artery. Moreover, the smooth muscle of these vessels does not respond directly to β-adrenergic- or cholinergic-receptor stimulation.
Persistent Identifierhttp://hdl.handle.net/10722/170979
ISSN
1998 Impact Factor: 3.077
2004 SCImago Journal Rankings: 1.102
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorO'rourke, STen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:41Z-
dc.date.available2012-10-30T06:11:41Z-
dc.date.issued1990en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1990, v. 259 n. 1 28-1, p. H156-H161en_US
dc.identifier.issn0002-9513en_US
dc.identifier.urihttp://hdl.handle.net/10722/170979-
dc.description.abstractThe purpose of this study was to characterize the adrenergic and cholinergic responsiveness of isolated rings of canine bronchial arteries. Electrical stimulation of the vessels produced frequency-dependent contractions that were inhibited by phenoxybenzamine, tetrodotoxin, and phentolamine but not by atropine. Norepinephrine caused concentration-dependent contractions of the rings; the concentration-response curve to norepinephrine was shifted to the right by phentolamine and prazosin, whereas rauwolscine had no effect. Isoproterenol, norepinephrine, tyramine, and electrical stimulation (in the presence of phentolamine) failed to elicit relaxation in rings contracted with prostaglandin F(2α). Contracted rings relaxed to acetylcholine in an endothelium- and concentration-dependent manner. At concentrations up to 10-4 M, acetylcholine did not evoke contractions in these tissues. Endothelium-dependent relaxation to acetylcholine was inhibited by atropine and 4-diphenyl-acetoxy-N-methyl piperidine methiodine but not by pirenzepine. These results suggest that α1-adrenoceptors mediate contraction to norepinephrine, and M3-muscarinic receptors mediate endothelium-dependent relaxation to acetylcholine in the canine bronchial artery. Moreover, the smooth muscle of these vessels does not respond directly to β-adrenergic- or cholinergic-receptor stimulation.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAtropine - Pharmacologyen_US
dc.subject.meshBronchial Arteries - Innervation - Physiologyen_US
dc.subject.meshDinoprost - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshParasympathetic Nervous System - Drug Effects - Physiologyen_US
dc.subject.meshPhenoxybenzamine - Pharmacologyen_US
dc.subject.meshPhentolamine - Pharmacologyen_US
dc.subject.meshPrazosin - Pharmacologyen_US
dc.subject.meshRegional Blood Flow - Drug Effectsen_US
dc.subject.meshSympathetic Nervous System - Drug Effects - Physiologyen_US
dc.subject.meshTetrodotoxin - Pharmacologyen_US
dc.subject.meshTyramine - Pharmacologyen_US
dc.titleAdrenergic and cholinergic responsiveness of isolated canine bronchial arteriesen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid2375402-
dc.identifier.scopuseid_2-s2.0-0025182211en_US
dc.identifier.volume259en_US
dc.identifier.issue1 28-1en_US
dc.identifier.spageH156en_US
dc.identifier.epageH161en_US
dc.identifier.isiWOS:A1990DQ45700024-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridO'Rourke, ST=7005313078en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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