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Conference Paper: The inducible nitric oxide synthase is impaired by thrombin in vascular smooth muscle cells

TitleThe inducible nitric oxide synthase is impaired by thrombin in vascular smooth muscle cells
Authors
KeywordsHirudin
Nitrite
Nitro-L-arginine
Rat aorta
Issue Date1992
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1992, v. 20 SUPPL. 12, p. S142-S144 How to Cite?
AbstractThe present study investigated whether or not thrombin may affect the induction of nitric oxide (NO) synthase caused by interleukin-1β in cultured smooth muscle cells (SMCs) from the rat aorta. The release of nitrite, an oxidation product of NO, from interleukin-1β-activated SMCs was inhibited by thrombin. The inhibitory effect of thrombin was prevented by hirudin, a thrombin inhibitor, and required the presence of thrombin during the induction period. Under bioassay conditions, the perfusate from interleukin- 1β-activated SMCs relaxed endothelium-denuded rat aortic rings precontracted with phenylephrine. The perfusate from untreated SMCs or cells exposed to thrombin alone or to interleukin-1β in combination with thrombin relaxed only minimally the detector blood vessel. These observations demonstrate that thrombin inhibits the production of NO by the inducible NO synthase in cultured vascular SMCs.
Persistent Identifierhttp://hdl.handle.net/10722/173508
ISSN
2021 Impact Factor: 3.271
2020 SCImago Journal Rankings: 0.762
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSchini, VBen_US
dc.contributor.authorCatovsky, Sen_US
dc.contributor.authorScottBurden, Ten_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:25Z-
dc.date.available2012-10-30T06:32:25Z-
dc.date.issued1992en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1992, v. 20 SUPPL. 12, p. S142-S144en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/173508-
dc.description.abstractThe present study investigated whether or not thrombin may affect the induction of nitric oxide (NO) synthase caused by interleukin-1β in cultured smooth muscle cells (SMCs) from the rat aorta. The release of nitrite, an oxidation product of NO, from interleukin-1β-activated SMCs was inhibited by thrombin. The inhibitory effect of thrombin was prevented by hirudin, a thrombin inhibitor, and required the presence of thrombin during the induction period. Under bioassay conditions, the perfusate from interleukin- 1β-activated SMCs relaxed endothelium-denuded rat aortic rings precontracted with phenylephrine. The perfusate from untreated SMCs or cells exposed to thrombin alone or to interleukin-1β in combination with thrombin relaxed only minimally the detector blood vessel. These observations demonstrate that thrombin inhibits the production of NO by the inducible NO synthase in cultured vascular SMCs.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.subjectHirudin-
dc.subjectNitrite-
dc.subjectNitro-L-arginine-
dc.subjectRat aorta-
dc.subject.meshAmino Acid Oxidoreductases - Antagonists & Inhibitors - Biosynthesisen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAortaen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEnzyme Inductionen_US
dc.subject.meshHirudins - Pharmacologyen_US
dc.subject.meshInterleukin-1 - Pharmacologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Drug Effects - Enzymologyen_US
dc.subject.meshNitric Oxide Synthaseen_US
dc.subject.meshNitroarginineen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshThrombin - Pharmacologyen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleThe inducible nitric oxide synthase is impaired by thrombin in vascular smooth muscle cellsen_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.doi10.1097/00005344-199204002-00040-
dc.identifier.pmid1282951-
dc.identifier.scopuseid_2-s2.0-0027078518en_US
dc.identifier.volume20en_US
dc.identifier.issueSUPPL. 12en_US
dc.identifier.spageS142en_US
dc.identifier.epageS144en_US
dc.identifier.isiWOS:A1992KF28300040-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridCatovsky, S=6602617293en_US
dc.identifier.scopusauthoridScottBurden, T=7004306459en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.issnl0160-2446-

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