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- Publisher Website: 10.1097/00005344-198003000-00004
- Scopus: eid_2-s2.0-0018861443
- PMID: 6171680
- WOS: WOS:A1980JL79200003
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Article: Inactivation of released norepinephrine in rat tail artery by neuronal uptake
Title | Inactivation of released norepinephrine in rat tail artery by neuronal uptake |
---|---|
Authors | |
Issue Date | 1980 |
Publisher | Lippincott 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/170601 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 0.610 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Webb, RC | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.contributor.author | Bohr, DF | en_US |
dc.date.accessioned | 2012-10-30T06:10:06Z | - |
dc.date.available | 2012-10-30T06:10:06Z | - |
dc.date.issued | 1980 | en_US |
dc.identifier.citation | Journal Of Cardiovascular Pharmacology, 1980, v. 2 n. 2, p. 121-132 | en_US |
dc.identifier.issn | 0160-2446 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170601 | - |
dc.description.abstract | The 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.language | eng | en_US |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ | en_US |
dc.relation.ispartof | Journal of Cardiovascular Pharmacology | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Arteries - Metabolism | en_US |
dc.subject.mesh | Cocaine - Pharmacology | en_US |
dc.subject.mesh | Denervation | en_US |
dc.subject.mesh | Electric Stimulation | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Muscle Contraction - Drug Effects | en_US |
dc.subject.mesh | Muscle, Smooth, Vascular - Drug Effects | en_US |
dc.subject.mesh | Neurons - Metabolism | en_US |
dc.subject.mesh | Norepinephrine - Metabolism - Pharmacology | en_US |
dc.subject.mesh | Phentolamine - Pharmacology | en_US |
dc.subject.mesh | Potassium - Pharmacology | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Tail - Blood Supply | en_US |
dc.title | Inactivation of released norepinephrine in rat tail artery by neuronal uptake | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1097/00005344-198003000-00004 | - |
dc.identifier.pmid | 6171680 | - |
dc.identifier.scopus | eid_2-s2.0-0018861443 | en_US |
dc.identifier.volume | 2 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 121 | en_US |
dc.identifier.epage | 132 | en_US |
dc.identifier.isi | WOS:A1980JL79200003 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Webb, RC=6603072737 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.scopusauthorid | Bohr, DF=7004979426 | en_US |
dc.identifier.issnl | 0160-2446 | - |