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Conference Paper: Mechanisms underlying the inhibitory interaction between the nitrovasodilator SIN-1 and the endothelium

TitleMechanisms underlying the inhibitory interaction between the nitrovasodilator SIN-1 and the endothelium
Authors
Issue Date1989
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1989, v. 14 SUPPL. 11, p. S86-S90 How to Cite?
AbstractExperiments were designed to determine the influence of the endothelium on the relaxing potency of the nitrovasodilator SIN-1. Rings of coronary arteries were suspended for isometric-tension recording in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% O2-5% CO2 and warmed to 37°C. The experiments were performed in the presence of indomethacin and propranolol in order to inhibit cyclooxygenase and β-adrenoceptors, respectively. In rings contracted with prostaglandin F(2α), SIN-1 caused concentration-dependent relaxations that were increased following endothelium removal. In rings denuded of endothelium, the relaxations evoked by SIN-1 were not affected by N(G)-monomethyl-L-arginine (L-NMMA, which inhibits the production of endothelium-derived relaxing factor), or by superoxide dismutase and catalase (scavengers of oxygen-derived free radicals), or by L-NMMA plus superoxide dismutase and catalase. In rings with endothelium, relaxations evoked by SIN-1 were increased significantly by L-NMMA or by superoxide dismutase and catalase, and were increased further by the combination of L-NMMA plus superoxide dismutase and catalase. The difference in potency of SIN-1 between arterial rings with and without endothelium was reduced by either L-NMMA or by superoxide dismutase and catalase, and was abolished by the combination of L-NMMA plus superoxide dismutase and catalase. Therefore, the inhibitory interaction between SIN-1 and the endothelium may result from an endothelium-dependent production of oxygen-derived free radicals that may inactivate the nitric oxide generated by SIN-1, and from an inhibitory interaction between SIN-1 and endothelium-derived relazxing factor, released under basal conditions.
Persistent Identifierhttp://hdl.handle.net/10722/173464
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:12Z-
dc.date.available2012-10-30T06:32:12Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1989, v. 14 SUPPL. 11, p. S86-S90en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/173464-
dc.description.abstractExperiments were designed to determine the influence of the endothelium on the relaxing potency of the nitrovasodilator SIN-1. Rings of coronary arteries were suspended for isometric-tension recording in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% O2-5% CO2 and warmed to 37°C. The experiments were performed in the presence of indomethacin and propranolol in order to inhibit cyclooxygenase and β-adrenoceptors, respectively. In rings contracted with prostaglandin F(2α), SIN-1 caused concentration-dependent relaxations that were increased following endothelium removal. In rings denuded of endothelium, the relaxations evoked by SIN-1 were not affected by N(G)-monomethyl-L-arginine (L-NMMA, which inhibits the production of endothelium-derived relaxing factor), or by superoxide dismutase and catalase (scavengers of oxygen-derived free radicals), or by L-NMMA plus superoxide dismutase and catalase. In rings with endothelium, relaxations evoked by SIN-1 were increased significantly by L-NMMA or by superoxide dismutase and catalase, and were increased further by the combination of L-NMMA plus superoxide dismutase and catalase. The difference in potency of SIN-1 between arterial rings with and without endothelium was reduced by either L-NMMA or by superoxide dismutase and catalase, and was abolished by the combination of L-NMMA plus superoxide dismutase and catalase. Therefore, the inhibitory interaction between SIN-1 and the endothelium may result from an endothelium-dependent production of oxygen-derived free radicals that may inactivate the nitric oxide generated by SIN-1, and from an inhibitory interaction between SIN-1 and endothelium-derived relazxing factor, released under basal conditions.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshFree Radicalsen_US
dc.subject.meshMaleen_US
dc.subject.meshMolsidomine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleMechanisms underlying the inhibitory interaction between the nitrovasodilator SIN-1 and the endotheliumen_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.doi10.1097/00005344-198914110-00016-
dc.identifier.pmid2484707-
dc.identifier.scopuseid_2-s2.0-0024828935en_US
dc.identifier.volume14en_US
dc.identifier.issueSUPPL. 11en_US
dc.identifier.spageS86en_US
dc.identifier.epageS90en_US
dc.identifier.isiWOS:A1989EC14200016-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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