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Conference Paper: G-proteins and endothelial responses

TitleG-proteins and endothelial responses
Authors
Issue Date1990
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
Blood Vessels, 1990, v. 27 n. 2-5, p. 218-229 How to Cite?
AbstractG-proteins are transducing proteins that couple a large number of membrane-bound receptors to a variety of intracellular effector systems. Pertussis toxin ADP-ribosylates certain G-proteins causing inhibition of their function. In porcine coronary arteries, pertussis toxin inhibited the endothelium-dependent relaxations evoked by alpha-2-adrenergic or serotonergic receptor stimulation, and by aggregating platelets or thrombin. Relaxations to nitric oxide and endothelium-dependent relaxations to bradykinin, adenosine diphosphate or A23187 were unaffected by the toxin. Therefore, certain endothelium-dependent relaxations are mediated by activation of a pertussis toxin-sensitive G-protein in the endothelial cells, most likely G(i)-protein. In porcine coronary arteries with regenerated endothelium (following in vivo denudation), the endothelium-dependent relaxations caused by the pertussis toxin-sensitive stimuli were reduced and were not further affected by pertussis toxin. Relaxations to be other stimuli were not altered by the regeneration process and were still not affected by the toxin. In regenerating endothelial cells there may be a selective impairment of the G-protein-dependent mechanism for releasing EDRF, which may predispose the blood vessel to vasospasm or the initiation of vascular disease.
Persistent Identifierhttp://hdl.handle.net/10722/173468
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:13Z-
dc.date.available2012-10-30T06:32:13Z-
dc.date.issued1990en_US
dc.identifier.citationBlood Vessels, 1990, v. 27 n. 2-5, p. 218-229en_US
dc.identifier.issn0303-6847en_US
dc.identifier.urihttp://hdl.handle.net/10722/173468-
dc.description.abstractG-proteins are transducing proteins that couple a large number of membrane-bound receptors to a variety of intracellular effector systems. Pertussis toxin ADP-ribosylates certain G-proteins causing inhibition of their function. In porcine coronary arteries, pertussis toxin inhibited the endothelium-dependent relaxations evoked by alpha-2-adrenergic or serotonergic receptor stimulation, and by aggregating platelets or thrombin. Relaxations to nitric oxide and endothelium-dependent relaxations to bradykinin, adenosine diphosphate or A23187 were unaffected by the toxin. Therefore, certain endothelium-dependent relaxations are mediated by activation of a pertussis toxin-sensitive G-protein in the endothelial cells, most likely G(i)-protein. In porcine coronary arteries with regenerated endothelium (following in vivo denudation), the endothelium-dependent relaxations caused by the pertussis toxin-sensitive stimuli were reduced and were not further affected by pertussis toxin. Relaxations to be other stimuli were not altered by the regeneration process and were still not affected by the toxin. In regenerating endothelial cells there may be a selective impairment of the G-protein-dependent mechanism for releasing EDRF, which may predispose the blood vessel to vasospasm or the initiation of vascular disease.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVRen_US
dc.relation.ispartofBlood Vesselsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCardiovascular Diseases - Pathologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Injuries - Metabolismen_US
dc.subject.meshGtp-Binding Proteins - Physiologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshPertussis Toxinen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.subject.meshVirulence Factors, Bordetella - Pharmacologyen_US
dc.titleG-proteins and endothelial responsesen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid2122922-
dc.identifier.scopuseid_2-s2.0-0025027155en_US
dc.identifier.volume27en_US
dc.identifier.issue2-5en_US
dc.identifier.spage218en_US
dc.identifier.epage229en_US
dc.identifier.isiWOS:A1990EJ15600017-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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