File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: G proteins and endothelium-dependent relaxations

TitleG proteins and endothelium-dependent relaxations
Authors
Issue Date1997
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
Journal Of Vascular Research, 1997, v. 34 n. 3, p. 175-185 How to Cite?
AbstractEndothelial cells control the tone of the underlying smooth muscle by releasing relaxing factors (nitric oxide, NO, prostacyclin and endothelium-derived hyperpolarizing factor). G proteins couple a number of endothelial cell receptors to the activation of NO synthase. Pertussis toxin selectively ADP-ribosylates certain G proteins (mainly G(i)). In the porcine coronary artery, pertussis toxin inhibits the release of NO evoked by certain (serotonin, α2-adrenergic agonists, leukotrienes, thrombin), but not all, (bradykinin, adenosine diphosphate) endothelium-dependent vasodilators. This suggests that both G(i) and G(q) proteins can couple receptor activation to the increase in endothelial Ca2+ concentration required to stimulate NO synthase. In arteries with regenerated endothelium and in cultured endothelial cells, the release of NO evoked by pertussis-toxin-sensitive mechanisms is severely reduced or absent, while the response to other endothelium-dependent agonists is normal. To judge from experiments with cultured endothelial cells, the curtailment in pertussis-toxin-sensitive release of NO is due to an abnormal function rather than a reduced presence of G(i) proteins, or a reduced sensitivity of the cell membrane receptor. The selective impairment of G(i) proteins in regenerated endothelial cells predisposes the blood vessel wall to vasospasm and to the initiation of the atherosclerotic process.
Persistent Identifierhttp://hdl.handle.net/10722/173530
ISSN
2015 Impact Factor: 2.186
2015 SCImago Journal Rankings: 1.119
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBoulanger, CMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:32Z-
dc.date.available2012-10-30T06:32:32Z-
dc.date.issued1997en_US
dc.identifier.citationJournal Of Vascular Research, 1997, v. 34 n. 3, p. 175-185en_US
dc.identifier.issn1018-1172en_US
dc.identifier.urihttp://hdl.handle.net/10722/173530-
dc.description.abstractEndothelial cells control the tone of the underlying smooth muscle by releasing relaxing factors (nitric oxide, NO, prostacyclin and endothelium-derived hyperpolarizing factor). G proteins couple a number of endothelial cell receptors to the activation of NO synthase. Pertussis toxin selectively ADP-ribosylates certain G proteins (mainly G(i)). In the porcine coronary artery, pertussis toxin inhibits the release of NO evoked by certain (serotonin, α2-adrenergic agonists, leukotrienes, thrombin), but not all, (bradykinin, adenosine diphosphate) endothelium-dependent vasodilators. This suggests that both G(i) and G(q) proteins can couple receptor activation to the increase in endothelial Ca2+ concentration required to stimulate NO synthase. In arteries with regenerated endothelium and in cultured endothelial cells, the release of NO evoked by pertussis-toxin-sensitive mechanisms is severely reduced or absent, while the response to other endothelium-dependent agonists is normal. To judge from experiments with cultured endothelial cells, the curtailment in pertussis-toxin-sensitive release of NO is due to an abnormal function rather than a reduced presence of G(i) proteins, or a reduced sensitivity of the cell membrane receptor. The selective impairment of G(i) proteins in regenerated endothelial cells predisposes the blood vessel wall to vasospasm and to the initiation of the atherosclerotic process.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.ispartofJournal of Vascular Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshEndothelium, Vascular - Physiology - Physiopathologyen_US
dc.subject.meshGtp-Binding Proteins - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshVasodilation - Physiologyen_US
dc.titleG proteins and endothelium-dependent relaxationsen_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.doi10.1159/000159221-
dc.identifier.pmid9226299-
dc.identifier.scopuseid_2-s2.0-0030962682en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030962682&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume34en_US
dc.identifier.issue3en_US
dc.identifier.spage175en_US
dc.identifier.epage185en_US
dc.identifier.isiWOS:A1997XK64400004-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats