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Article: Balloon injury and interleukin-1 β induce nitric oxide synthase activity in rat carotid arteries

TitleBalloon injury and interleukin-1 β induce nitric oxide synthase activity in rat carotid arteries
Authors
Issue Date1992
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1992, v. 71 n. 2, p. 331-338 How to Cite?
AbstractExperiments were performed to investigate whether balloon injury induces nitric oxide synthase activity in the blood vessel wall. Contractions to phenylephrine were compared in left carotid arteries of the rat, previously injured by balloon catheterization and excised either immediately (t=0), 6, or 24 hours after the procedure, with those in control right carotid arteries (with and without endothelium). Phenylephrine evoked comparable concentration-dependent contractions in balloon-injured (t=0) and control carotid arteries without endothelium, whereas those in control arteries with endothelium were depressed. In the balloon-injured carotid arteries (6 and 24 hours), the concentration-contraction curves to phenylephrine were shifted to the right compared with those observed in balloon-injured arteries (t=0). In balloon-injured carotid arteries (6 hours), the hyporeactivity to phenylephrine was enhanced by superoxide dismutase. In balloon-injured carotid arteries (24 hours), nitro-L-arginine and methylene blue restored full contractions, whereas superoxide dismutase potentiated the hyporesponsiveness to phenylephrine. The depressed contractions were associated with a concomitant increase in the basal level of cGMP; this production was abolished by nitro-L-arginine. The depression of the concentration-contraction curves to phenylephrine and the increase of the tissue level of cGMP induced by interleukin-1 β (4 hours) were more pronounced in balloon-injured arteries (24 hours) than in control arteries without endothelium. The effects of interleukin-1 β were inhibited by nitro- L-arginine. These observations indicate that in vivo endothelial injury of the rat carotid arteries induces the production of nitric oxide from L- arginine in the blood vessel wall, an effect which is potentiated by interleukin-1 β.
Persistent Identifierhttp://hdl.handle.net/10722/171061
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJoly, GAen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:02Z-
dc.date.available2012-10-30T06:12:02Z-
dc.date.issued1992en_US
dc.identifier.citationCirculation Research, 1992, v. 71 n. 2, p. 331-338en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/171061-
dc.description.abstractExperiments were performed to investigate whether balloon injury induces nitric oxide synthase activity in the blood vessel wall. Contractions to phenylephrine were compared in left carotid arteries of the rat, previously injured by balloon catheterization and excised either immediately (t=0), 6, or 24 hours after the procedure, with those in control right carotid arteries (with and without endothelium). Phenylephrine evoked comparable concentration-dependent contractions in balloon-injured (t=0) and control carotid arteries without endothelium, whereas those in control arteries with endothelium were depressed. In the balloon-injured carotid arteries (6 and 24 hours), the concentration-contraction curves to phenylephrine were shifted to the right compared with those observed in balloon-injured arteries (t=0). In balloon-injured carotid arteries (6 hours), the hyporeactivity to phenylephrine was enhanced by superoxide dismutase. In balloon-injured carotid arteries (24 hours), nitro-L-arginine and methylene blue restored full contractions, whereas superoxide dismutase potentiated the hyporesponsiveness to phenylephrine. The depressed contractions were associated with a concomitant increase in the basal level of cGMP; this production was abolished by nitro-L-arginine. The depression of the concentration-contraction curves to phenylephrine and the increase of the tissue level of cGMP induced by interleukin-1 β (4 hours) were more pronounced in balloon-injured arteries (24 hours) than in control arteries without endothelium. The effects of interleukin-1 β were inhibited by nitro- L-arginine. These observations indicate that in vivo endothelial injury of the rat carotid arteries induces the production of nitric oxide from L- arginine in the blood vessel wall, an effect which is potentiated by interleukin-1 β.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAmino Acid Oxidoreductases - Biosynthesisen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshBalloon Dilation - Adverse Effectsen_US
dc.subject.meshCarotid Arteries - Enzymologyen_US
dc.subject.meshCarotid Artery Injuriesen_US
dc.subject.meshCyclic Gmp - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Enzymology - Injuriesen_US
dc.subject.meshInterleukin-1 - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxide Synthaseen_US
dc.subject.meshNitroarginineen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Strainsen_US
dc.subject.meshSuperoxide Dismutase - Pharmacologyen_US
dc.titleBalloon injury and interleukin-1 β induce nitric oxide synthase activity in rat carotid arteriesen_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.pmid1378360-
dc.identifier.scopuseid_2-s2.0-0026659727en_US
dc.identifier.volume71en_US
dc.identifier.issue2en_US
dc.identifier.spage331en_US
dc.identifier.epage338en_US
dc.identifier.isiWOS:A1992JE93500010-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridJoly, GA=7005110329en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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