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Article: Eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1β in cultured vascular smooth muscle cells

TitleEicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1β in cultured vascular smooth muscle cells
Authors
Issue Date1993
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
Journal Of Vascular Research, 1993, v. 30 n. 4, p. 209-217 How to Cite?
AbstractExperiments were designed to determine whether the ω3-unsaturated fatty acid eicosapentaenoic acid affects the production of nitric oxide evoked by interleukin-1β in cultured vascular smooth muscle cells. Incubation of cultured rat or human aortic smooth muscle cells with interleukin-1β evoked a time- and concentration-dependent release of nitrite, an oxidation product of nitric oxide. The exposure of cells to interleukin-1β in combination with eicosapentaenoic acid caused a significantly larger production of nitrite than that evoked by the cytokine alone. The potentiation by eicosapentaenoic acid was concentration-dependent. The production of nitrite evoked by equieffective concentrations of interleukin-1β in the presence and absence of eicosapentaenoic acid were inhibited to a similar extent by nitro L- arginine (an inhibitor of nitric oxide synthase), transforming growth factor β1, platelet-derived growth factor(AB) and thrombin. The addition of interleukin-1β-activated smooth muscle cells to suspensions of washed and indomethacin-treated platelets inhibited the aggregation caused by thrombin. The inhibitory effect was enhanced when the smooth muscle cells were exposed to the cytokine in the presence of eicosapentaenoic acid prior to the experiment. Smooth muscle cells exposed to interleukin-1β and eicosapentaenoic acid did not affect platelet aggregation in the presence of oxyhemoglobin or methylene blue. Untreated cells or cells exposed to the fatty acid alone did not have such effects. These observations suggest that eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1β in vascular smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/171083
ISSN
2015 Impact Factor: 2.186
2015 SCImago Journal Rankings: 1.119
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSchini, VBen_US
dc.contributor.authorDurante, Wen_US
dc.contributor.authorCatovsky, Sen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:08Z-
dc.date.available2012-10-30T06:12:08Z-
dc.date.issued1993en_US
dc.identifier.citationJournal Of Vascular Research, 1993, v. 30 n. 4, p. 209-217en_US
dc.identifier.issn1018-1172en_US
dc.identifier.urihttp://hdl.handle.net/10722/171083-
dc.description.abstractExperiments were designed to determine whether the ω3-unsaturated fatty acid eicosapentaenoic acid affects the production of nitric oxide evoked by interleukin-1β in cultured vascular smooth muscle cells. Incubation of cultured rat or human aortic smooth muscle cells with interleukin-1β evoked a time- and concentration-dependent release of nitrite, an oxidation product of nitric oxide. The exposure of cells to interleukin-1β in combination with eicosapentaenoic acid caused a significantly larger production of nitrite than that evoked by the cytokine alone. The potentiation by eicosapentaenoic acid was concentration-dependent. The production of nitrite evoked by equieffective concentrations of interleukin-1β in the presence and absence of eicosapentaenoic acid were inhibited to a similar extent by nitro L- arginine (an inhibitor of nitric oxide synthase), transforming growth factor β1, platelet-derived growth factor(AB) and thrombin. The addition of interleukin-1β-activated smooth muscle cells to suspensions of washed and indomethacin-treated platelets inhibited the aggregation caused by thrombin. The inhibitory effect was enhanced when the smooth muscle cells were exposed to the cytokine in the presence of eicosapentaenoic acid prior to the experiment. Smooth muscle cells exposed to interleukin-1β and eicosapentaenoic acid did not affect platelet aggregation in the presence of oxyhemoglobin or methylene blue. Untreated cells or cells exposed to the fatty acid alone did not have such effects. These observations suggest that eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1β in vascular smooth muscle.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.meshAorta - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshArginine - Pharmacologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEicosapentaenoic Acid - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInterleukin-1 - Pharmacologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitrites - Metabolismen_US
dc.subject.meshPlatelet Aggregation - Drug Effectsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.titleEicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1β in cultured vascular smooth muscle cellsen_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.doi10.1159/000158996-
dc.identifier.pmid8357951-
dc.identifier.scopuseid_2-s2.0-0027181481en_US
dc.identifier.volume30en_US
dc.identifier.issue4en_US
dc.identifier.spage209en_US
dc.identifier.epage217en_US
dc.identifier.isiWOS:A1993LW11800004-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridDurante, W=7006946922en_US
dc.identifier.scopusauthoridCatovsky, S=6602617293en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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