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Article: Plasmin potentiates induction of nitric oxide synthesis by interleukin- 1β in vascular smooth muscle cells

TitlePlasmin potentiates induction of nitric oxide synthesis by interleukin- 1β in vascular smooth muscle cells
Authors
Issue Date1993
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1993, v. 264 n. 2 33-2, p. H617-H624 How to Cite?
AbstractExperiments were performed to examine the effect of the major fibrinolytic protease, plasmin, on the production of nitric oxide from interleukin-1β (IL-1β)-treated cultured human and rat aortic smooth muscle cells. Incubation of vascular smooth muscle cells with IL-1β resulted in significant accumulation of nitrite and nitrate in the culture media. Plasmin, either added exogenously or generated by the reaction of tissue plasminogen activator with plasminogen, potentiated the IL-1β-mediated release of nitrite and nitrate from smooth muscle cells in a concentration- dependent manner, without affecting the production of nitrite and nitrate from cells untreated with IL-1β. This potentiating effect was abolished when plasmin was incubated with the protease inhibitor, α2-antiplasmin. The perfusates from columns containing IL-1β-treated smooth muscle cells relaxed detector blood vessels without endothelium, and the addition of IL-1β- treated smooth muscle cells to suspensions of indomethacin-treated platelets inhibited their aggregation. Untreated smooth muscle cells or cells treated with plasmin alone did not have such effects. However, the simultaneous treatment of smooth muscle cells with IL-1β and plasmin markedly enhanced both the relaxing activities of the perfusates and the inhibition of platelet aggregation. Treatment of smooth muscle cells with N(G)-nitro-L-arginine inhibited the cytokine-mediated effects as well as the potentiating effect of plasmin. These results demonstrate that plasmin can enhance the production of nitric oxide by IL-1β-treated vascular smooth muscle cells.
Persistent Identifierhttp://hdl.handle.net/10722/171109
ISSN
1998 Impact Factor: 3.077
2004 SCImago Journal Rankings: 1.102
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDurante, Wen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorCatovsky, Sen_US
dc.contributor.authorKroll, MHen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorSchafer, AIen_US
dc.date.accessioned2012-10-30T06:12:13Z-
dc.date.available2012-10-30T06:12:13Z-
dc.date.issued1993en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1993, v. 264 n. 2 33-2, p. H617-H624en_US
dc.identifier.issn0002-9513en_US
dc.identifier.urihttp://hdl.handle.net/10722/171109-
dc.description.abstractExperiments were performed to examine the effect of the major fibrinolytic protease, plasmin, on the production of nitric oxide from interleukin-1β (IL-1β)-treated cultured human and rat aortic smooth muscle cells. Incubation of vascular smooth muscle cells with IL-1β resulted in significant accumulation of nitrite and nitrate in the culture media. Plasmin, either added exogenously or generated by the reaction of tissue plasminogen activator with plasminogen, potentiated the IL-1β-mediated release of nitrite and nitrate from smooth muscle cells in a concentration- dependent manner, without affecting the production of nitrite and nitrate from cells untreated with IL-1β. This potentiating effect was abolished when plasmin was incubated with the protease inhibitor, α2-antiplasmin. The perfusates from columns containing IL-1β-treated smooth muscle cells relaxed detector blood vessels without endothelium, and the addition of IL-1β- treated smooth muscle cells to suspensions of indomethacin-treated platelets inhibited their aggregation. Untreated smooth muscle cells or cells treated with plasmin alone did not have such effects. However, the simultaneous treatment of smooth muscle cells with IL-1β and plasmin markedly enhanced both the relaxing activities of the perfusates and the inhibition of platelet aggregation. Treatment of smooth muscle cells with N(G)-nitro-L-arginine inhibited the cytokine-mediated effects as well as the potentiating effect of plasmin. These results demonstrate that plasmin can enhance the production of nitric oxide by IL-1β-treated vascular smooth muscle cells.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Assayen_US
dc.subject.meshBlood Platelets - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshFibrinolysin - 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.meshPlasminogen - Pharmacologyen_US
dc.subject.meshPlatelet Aggregation - Drug Effectsen_US
dc.subject.meshRatsen_US
dc.subject.meshThrombin - Pharmacologyen_US
dc.subject.meshTissue Plasminogen Activator - Pharmacologyen_US
dc.subject.meshVasodilationen_US
dc.titlePlasmin potentiates induction of nitric oxide synthesis by interleukin- 1β in 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.pmid8447474-
dc.identifier.scopuseid_2-s2.0-0027468889en_US
dc.identifier.volume264en_US
dc.identifier.issue2 33-2en_US
dc.identifier.spageH617en_US
dc.identifier.epageH624en_US
dc.identifier.isiWOS:A1993KN68100048-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDurante, W=7006946922en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridCatovsky, S=6602617293en_US
dc.identifier.scopusauthoridKroll, MH=7102187905en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridSchafer, AI=7202243976en_US

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