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Article: Cholera toxin augments the release of endothelium-derived relaxing factor evoked by bradykinin and the calcium ionophore A23187

TitleCholera toxin augments the release of endothelium-derived relaxing factor evoked by bradykinin and the calcium ionophore A23187
Authors
Issue Date1992
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/vph
Citation
General Pharmacology, 1992, v. 23 n. 1, p. 27-31 How to Cite?
AbstractExperiments were designed to examine the effect of cholera toxin and forskolin on the release of relaxing factor(s) from superfused cultured endothelial cells under basal conditions and upon stimulation with bradykinin, adenosine diphosphate or the calcium ionophore A23187. Exposure of cultured porcine aortic endothelial cells to cholera toxin (30 μg/ml, for 3 hr) and forskolin (10-6 M, for 45 min) significantly increased the intracellular content in cyclic AMP. Cholera toxin but not forskolin stimulated the accumulation of cyclic GMP. Exposure to cholera toxin did not modify the basal release of endothelium-derived relaxing factor nor that induced by adenosine diphosphate, but significantly increased that evoked by bradykinin and the calcium ionophore A23187. Forskolin did not significantly affect the basal or the stimulated release of endothelium-derived relaxing factor. These results suggest that cholera toxin potentiates the release of endothelium-derived relaxing factor (presumably nitric oxide) from endothelial cells by a mechanism other than augmented production of cyclic AMP.
Persistent Identifierhttp://hdl.handle.net/10722/171048
ISSN
2002 Impact Factor: 0.591
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBoulanger, CMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:59Z-
dc.date.available2012-10-30T06:11:59Z-
dc.date.issued1992en_US
dc.identifier.citationGeneral Pharmacology, 1992, v. 23 n. 1, p. 27-31en_US
dc.identifier.issn0306-3623en_US
dc.identifier.urihttp://hdl.handle.net/10722/171048-
dc.description.abstractExperiments were designed to examine the effect of cholera toxin and forskolin on the release of relaxing factor(s) from superfused cultured endothelial cells under basal conditions and upon stimulation with bradykinin, adenosine diphosphate or the calcium ionophore A23187. Exposure of cultured porcine aortic endothelial cells to cholera toxin (30 μg/ml, for 3 hr) and forskolin (10-6 M, for 45 min) significantly increased the intracellular content in cyclic AMP. Cholera toxin but not forskolin stimulated the accumulation of cyclic GMP. Exposure to cholera toxin did not modify the basal release of endothelium-derived relaxing factor nor that induced by adenosine diphosphate, but significantly increased that evoked by bradykinin and the calcium ionophore A23187. Forskolin did not significantly affect the basal or the stimulated release of endothelium-derived relaxing factor. These results suggest that cholera toxin potentiates the release of endothelium-derived relaxing factor (presumably nitric oxide) from endothelial cells by a mechanism other than augmented production of cyclic AMP.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/vphen_US
dc.relation.ispartofGeneral Pharmacologyen_US
dc.subject.meshAdenosine Diphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCholera Toxin - Pharmacologyen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshCyclic Gmp - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelium, Vascular - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshSwineen_US
dc.titleCholera toxin augments the release of endothelium-derived relaxing factor evoked by bradykinin and the calcium ionophore A23187en_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.doi10.1016/0306-3623(92)90042-Ien_US
dc.identifier.pmid1317311-
dc.identifier.scopuseid_2-s2.0-0026529191en_US
dc.identifier.volume23en_US
dc.identifier.issue1en_US
dc.identifier.spage27en_US
dc.identifier.epage31en_US
dc.identifier.isiWOS:A1992GY39200005-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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