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Article: Inactivation of released norepinephrine in rat tail artery by neuronal uptake

TitleInactivation of released norepinephrine in rat tail artery by neuronal uptake
Authors
Issue Date1980
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1980, v. 2 n. 2, p. 121-132 How to Cite?
AbstractThe relationship between adrenergic nerve activity and neuronal uptake was investigated. Helically cut strips of rat tail artery were mounted in organ chambers and isometric contractions were recorded. Spontaneous contractions were occasionally observed and these contractions were blocked by phentolamine. Cumulative addition of cocaine produced contractions of the strips. These contractions were blocked by phentolamine and reduced after denervation with 6-hydroxydopamine. Cocaine potentiated the contractile responses to exogenous norepinephrine and caused a shift to the left in the concentration-response curve. Contractions in response to low-frequency field stimulation were potentiated by cocaine; contractions produced by high frequencies were not altered by the drug. Cocaine had no effect on contractions produced by depolarization of the prejunctional membrane with high potassium. The relative rates of relaxation following high- and low-frequency stimulation were increased similarly by cocaine. The results indicate (1) the spontaneous activity of rat tail artery is related to the leakage of norepinephrine from nerve endings; (2) contraction in response to cocaine alone probably results from inhibition of neuronal uptake and the release of endogenous norepinephrine; and (3) the amine uptake mechanism is not operative during depolarization of prejunctional membrane.
Persistent Identifierhttp://hdl.handle.net/10722/170601
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWebb, RCen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorBohr, DFen_US
dc.date.accessioned2012-10-30T06:10:06Z-
dc.date.available2012-10-30T06:10:06Z-
dc.date.issued1980en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1980, v. 2 n. 2, p. 121-132en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/170601-
dc.description.abstractThe relationship between adrenergic nerve activity and neuronal uptake was investigated. Helically cut strips of rat tail artery were mounted in organ chambers and isometric contractions were recorded. Spontaneous contractions were occasionally observed and these contractions were blocked by phentolamine. Cumulative addition of cocaine produced contractions of the strips. These contractions were blocked by phentolamine and reduced after denervation with 6-hydroxydopamine. Cocaine potentiated the contractile responses to exogenous norepinephrine and caused a shift to the left in the concentration-response curve. Contractions in response to low-frequency field stimulation were potentiated by cocaine; contractions produced by high frequencies were not altered by the drug. Cocaine had no effect on contractions produced by depolarization of the prejunctional membrane with high potassium. The relative rates of relaxation following high- and low-frequency stimulation were increased similarly by cocaine. The results indicate (1) the spontaneous activity of rat tail artery is related to the leakage of norepinephrine from nerve endings; (2) contraction in response to cocaine alone probably results from inhibition of neuronal uptake and the release of endogenous norepinephrine; and (3) the amine uptake mechanism is not operative during depolarization of prejunctional membrane.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.subject.meshAnimalsen_US
dc.subject.meshArteries - Metabolismen_US
dc.subject.meshCocaine - Pharmacologyen_US
dc.subject.meshDenervationen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNeurons - Metabolismen_US
dc.subject.meshNorepinephrine - Metabolism - Pharmacologyen_US
dc.subject.meshPhentolamine - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshTail - Blood Supplyen_US
dc.titleInactivation of released norepinephrine in rat tail artery by neuronal uptakeen_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.doi10.1097/00005344-198003000-00004-
dc.identifier.pmid6171680-
dc.identifier.scopuseid_2-s2.0-0018861443en_US
dc.identifier.volume2en_US
dc.identifier.issue2en_US
dc.identifier.spage121en_US
dc.identifier.epage132en_US
dc.identifier.isiWOS:A1980JL79200003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWebb, RC=6603072737en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridBohr, DF=7004979426en_US

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