Inactivation of released norepinephrine in rat tail artery by neuronal uptake

R. C. Webb, P. M. Vanhoutte, D. F. Bohr

Research output: Contribution to journalArticle

20 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)121-132
Number of pages12
JournalJournal of Cardiovascular Pharmacology
Volume2
Issue number2
DOIs
StatePublished - Jan 1 1980
Externally publishedYes

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Inactivation of released norepinephrine in rat tail artery by neuronal uptake'. Together they form a unique fingerprint.

  • Cite this