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Article: Endothelial vasomotor tone: Role of the G-proteins | Vasomotricite d'origine endotheliale. Role des proteines G

TitleEndothelial vasomotor tone: Role of the G-proteins | Vasomotricite d'origine endotheliale. Role des proteines G
Authors
Issue Date1997
PublisherJohn Libbey Eurotext. The Journal's web site is located at http://www.revue-stv.com
Citation
Sang Thrombose Vaisseaux, 1997, v. 9 n. 1, p. 22-30 How to Cite?
AbstractEndothelial cell controls the tone of the underlying smooth muscle by releasing relaxing factors: nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor (EDHF). G-proteins couple a number of endothelial cell receptors to the activation of NO synthase. Pertussis toxin ADP-ribosylates selectively certain G-proteins (mainly Gi). In the porcine coronary artery, pertussis toxin inhibits the release of NO induced by certain (serotonin, α2-adrenergic agonists, leukotrienes, thrombin) but not all (bradykinin, adenosine diphosphate) endothelium-dependent vasodilators. This suggests that both Gi and Gp-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 by the pertussis toxin sensitive mechanism is reduced severely or is 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 abnormal function of rather than reduced presence of Gi proteins, or to reduced sensitivity of the cell membrane receptor. The selective impairment of Gi-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/10722/171200
ISSN
2013 Impact Factor: 0.011
2015 SCImago Journal Rankings: 0.107
References

 

DC FieldValueLanguage
dc.contributor.authorBoulanger, CMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:39Z-
dc.date.available2012-10-30T06:12:39Z-
dc.date.issued1997en_US
dc.identifier.citationSang Thrombose Vaisseaux, 1997, v. 9 n. 1, p. 22-30en_US
dc.identifier.issn0999-7385en_US
dc.identifier.urihttp://hdl.handle.net/10722/171200-
dc.description.abstractEndothelial cell controls the tone of the underlying smooth muscle by releasing relaxing factors: nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor (EDHF). G-proteins couple a number of endothelial cell receptors to the activation of NO synthase. Pertussis toxin ADP-ribosylates selectively certain G-proteins (mainly Gi). In the porcine coronary artery, pertussis toxin inhibits the release of NO induced by certain (serotonin, α2-adrenergic agonists, leukotrienes, thrombin) but not all (bradykinin, adenosine diphosphate) endothelium-dependent vasodilators. This suggests that both Gi and Gp-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 by the pertussis toxin sensitive mechanism is reduced severely or is 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 abnormal function of rather than reduced presence of Gi proteins, or to reduced sensitivity of the cell membrane receptor. The selective impairment of Gi-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.publisherJohn Libbey Eurotext. The Journal's web site is located at http://www.revue-stv.comen_US
dc.relation.ispartofSang Thrombose Vaisseauxen_US
dc.titleEndothelial vasomotor tone: Role of the G-proteins | Vasomotricite d'origine endotheliale. Role des proteines Gen_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.scopuseid_2-s2.0-0030887884en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030887884&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume9en_US
dc.identifier.issue1en_US
dc.identifier.spage22en_US
dc.identifier.epage30en_US
dc.publisher.placeFranceen_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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