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Article: Platelet inhibition by an L-arginine-derived substance released by IL-1β-treated vascular smooth muscle cells

TitlePlatelet inhibition by an L-arginine-derived substance released by IL-1β-treated vascular smooth muscle cells
Authors
Issue Date1991
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1991, v. 261 n. 6 30-6, p. H2024-H2030 How to Cite?
AbstractExperiments were performed to examine whether stimulation of cultured vascular smooth muscle cells by interleukin (IL)-1β would induce platelet inhibitory properties of these cells. Incubation of platelets with untreated rat aortic smooth muscle cells had no effect on thrombin-induced platelet aggregation. In contrast, incubation of platelets with IL-1β-pretreated smooth muscle cells or the perfusate from such cells resulted in the inhibition of thrombin-induced platelet aggregation. This effect was potentiated by superoxide dismutase and reversed by incubating the IL-1β-treated smooth muscle cells with N(G)-nitro-L-arginine (L-NNA) or by treating the platelets with methylene blue. Cytokine-treated smooth muscle cells inhibited thrombin-stimulated changes in platelet cytosolic ionized calcium, whereas untreated cells were without effect. Incubating platelets with IL-1β-treated smooth muscle cells resulted in a 10-fold increase in platelet guanosine 3',5'-cyclic monophosphate (cGMP) levels, whereas untreated smooth muscle cells had no effect. The elevation of platelet cGMP induced by the IL-1β-treated smooth muscle cells was prevented by exposing the cytokine-treated cells to L-NNA or by treating platelets with methylene blue. Treatment of smooth muscle cells with IL-1β also resulted in an eightfold increase in nitrite production, which was blocked when the cells were incubated with L-NNA. The addition of cycloheximide to smooth muscle cells during their incubation with IL-1β completely inhibited smooth muscle cell nitrite production, the effects of the smooth muscle cells on platelet cGMP levels, and platelet responses to thrombin. These results demonstrate that vascular smooth muscle cells exposed to inflammatory mediators can release platelet inhibitory nitric oxide.
Persistent Identifierhttp://hdl.handle.net/10722/171037
ISSN
1998 Impact Factor: 3.077
2004 SCImago Journal Rankings: 1.102

 

DC FieldValueLanguage
dc.contributor.authorDurante, Wen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorScottBurden, Ten_US
dc.contributor.authorJunquero, DCen_US
dc.contributor.authorKroll, MHen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorSchafer, AIen_US
dc.date.accessioned2012-10-30T06:11:56Z-
dc.date.available2012-10-30T06:11:56Z-
dc.date.issued1991en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1991, v. 261 n. 6 30-6, p. H2024-H2030en_US
dc.identifier.issn0002-9513en_US
dc.identifier.urihttp://hdl.handle.net/10722/171037-
dc.description.abstractExperiments were performed to examine whether stimulation of cultured vascular smooth muscle cells by interleukin (IL)-1β would induce platelet inhibitory properties of these cells. Incubation of platelets with untreated rat aortic smooth muscle cells had no effect on thrombin-induced platelet aggregation. In contrast, incubation of platelets with IL-1β-pretreated smooth muscle cells or the perfusate from such cells resulted in the inhibition of thrombin-induced platelet aggregation. This effect was potentiated by superoxide dismutase and reversed by incubating the IL-1β-treated smooth muscle cells with N(G)-nitro-L-arginine (L-NNA) or by treating the platelets with methylene blue. Cytokine-treated smooth muscle cells inhibited thrombin-stimulated changes in platelet cytosolic ionized calcium, whereas untreated cells were without effect. Incubating platelets with IL-1β-treated smooth muscle cells resulted in a 10-fold increase in platelet guanosine 3',5'-cyclic monophosphate (cGMP) levels, whereas untreated smooth muscle cells had no effect. The elevation of platelet cGMP induced by the IL-1β-treated smooth muscle cells was prevented by exposing the cytokine-treated cells to L-NNA or by treating platelets with methylene blue. Treatment of smooth muscle cells with IL-1β also resulted in an eightfold increase in nitrite production, which was blocked when the cells were incubated with L-NNA. The addition of cycloheximide to smooth muscle cells during their incubation with IL-1β completely inhibited smooth muscle cell nitrite production, the effects of the smooth muscle cells on platelet cGMP levels, and platelet responses to thrombin. These results demonstrate that vascular smooth muscle cells exposed to inflammatory mediators can release platelet inhibitory nitric oxide.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.meshAorta, Thoracicen_US
dc.subject.meshArginine - Analogs & Derivatives - Metabolism - Pharmacologyen_US
dc.subject.meshBlood Platelets - Drug Effects - Metabolismen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyclic Gmp - Blooden_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshInterleukin-1 - Pharmacologyen_US
dc.subject.meshMethylene Blue - Pharmacologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Metabolismen_US
dc.subject.meshNitric Oxide - Metabolism - Pharmacologyen_US
dc.subject.meshNitroarginineen_US
dc.subject.meshPlatelet Aggregation - Drug Effectsen_US
dc.subject.meshPlatelet Aggregation Inhibitors - Metabolism - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshSuperoxide Dismutase - Pharmacologyen_US
dc.subject.meshThrombin - Pharmacologyen_US
dc.titlePlatelet inhibition by an L-arginine-derived substance released by IL-1β-treated 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.pmid1661096-
dc.identifier.scopuseid_2-s2.0-0026329415en_US
dc.identifier.volume261en_US
dc.identifier.issue6 30-6en_US
dc.identifier.spageH2024en_US
dc.identifier.epageH2030en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDurante, W=7006946922en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridScottBurden, T=7004306459en_US
dc.identifier.scopusauthoridJunquero, DC=26643025500en_US
dc.identifier.scopusauthoridKroll, MH=7102187905en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridSchafer, AI=7202243976en_US

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