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Article: Pertussis toxin inhibits endothelium-dependent relaxations to certain agonists in porcine coronary arteries

TitlePertussis toxin inhibits endothelium-dependent relaxations to certain agonists in porcine coronary arteries
Authors
Issue Date1989
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 1989, v. 408, p. 549-560 How to Cite?
AbstractPertussis toxin inactivates G(i)-protein, which mediates the inhibitory effects of receptors on adenylate cyclase. The effects of the toxin on endothelium-dependent and independent relaxations were determined in porcine coronary arteries. Arterial rings (with and without endothelium) were suspended for isometric tension recording in organ chambers filled with modified Krebs-Ringer bicarbonate solution (maintained at 37°C, gassed with 95% O2 and 5% CO2). Incubation of the tissues with pertussis toxin (100 ng/ml for 60 min) virtually abolished the endothelium-dependent relaxations produced by the α2-adrenergic agonist, UK 14304, and by 5-hydroxytryptamine. Endothelium-dependent relaxations to thrombin and to aggregating platelets were markedly reduced, whereas those produced by bradykinin were only minimally affected. Endothelium-dependent responses produced by the calcium ionophore (A23187) and by adenosine diphosphate were not altered by pertussis toxin. Pertussis toxin did not affect the direct, endothelium-independent relaxations produced by nitric oxide, or by adenosine diphosphate. These experiments demonstrate that pertussis toxin interferes with the release of endothelium-derived relaxing factor(s) evoked by certain, but not all, endothelial activators. The release of endothelium-derived relaxing factor(s) may occur through different pathways involving G(i)-protein-dependent and independent mechanisms.
Persistent Identifierhttp://hdl.handle.net/10722/170948
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorShimokawa, Hen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:34Z-
dc.date.available2012-10-30T06:11:34Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of Physiology, 1989, v. 408, p. 549-560en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/170948-
dc.description.abstractPertussis toxin inactivates G(i)-protein, which mediates the inhibitory effects of receptors on adenylate cyclase. The effects of the toxin on endothelium-dependent and independent relaxations were determined in porcine coronary arteries. Arterial rings (with and without endothelium) were suspended for isometric tension recording in organ chambers filled with modified Krebs-Ringer bicarbonate solution (maintained at 37°C, gassed with 95% O2 and 5% CO2). Incubation of the tissues with pertussis toxin (100 ng/ml for 60 min) virtually abolished the endothelium-dependent relaxations produced by the α2-adrenergic agonist, UK 14304, and by 5-hydroxytryptamine. Endothelium-dependent relaxations to thrombin and to aggregating platelets were markedly reduced, whereas those produced by bradykinin were only minimally affected. Endothelium-dependent responses produced by the calcium ionophore (A23187) and by adenosine diphosphate were not altered by pertussis toxin. Pertussis toxin did not affect the direct, endothelium-independent relaxations produced by nitric oxide, or by adenosine diphosphate. These experiments demonstrate that pertussis toxin interferes with the release of endothelium-derived relaxing factor(s) evoked by certain, but not all, endothelial activators. The release of endothelium-derived relaxing factor(s) may occur through different pathways involving G(i)-protein-dependent and independent mechanisms.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_US
dc.relation.ispartofJournal of Physiologyen_US
dc.subject.meshAdenylate Cyclase Toxinen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vesselsen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMethylene Blue - Pharmacologyen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshOxyhemoglobinsen_US
dc.subject.meshPertussis Toxinen_US
dc.subject.meshPlatelet Aggregationen_US
dc.subject.meshQuinoxalines - Pharmacologyen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.subject.meshSwineen_US
dc.subject.meshThrombinen_US
dc.subject.meshVirulence Factors, Bordetella - Pharmacologyen_US
dc.titlePertussis toxin inhibits endothelium-dependent relaxations to certain agonists in porcine coronary 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.pmid2778738-
dc.identifier.scopuseid_2-s2.0-0024495576en_US
dc.identifier.volume408en_US
dc.identifier.spage549en_US
dc.identifier.epage560en_US
dc.identifier.isiWOS:A1989R860200034-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridShimokawa, H=16684837100en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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