Inactivation of released norepinephrine in rat tail artery by neuronal uptake

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

Research output: Contribution to journalArticle

20 Citations (Scopus)

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

Fingerprint

Cocaine
Tail
Norepinephrine
Arteries
Phentolamine
Isometric Contraction
Membranes
Nerve Endings
Oxidopamine
Denervation
Adrenergic Agents
Amines
Potassium
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Inactivation of released norepinephrine in rat tail artery by neuronal uptake. / Webb, R Clinton; Vanhoutte, P. M.; Bohr, D. F.

In: Journal of Cardiovascular Pharmacology, Vol. 2, No. 2, 01.01.1980, p. 121-132.

Research output: Contribution to journalArticle

@article{c6aef20451654f9b85fa677a631270c5,
title = "Inactivation of released norepinephrine in rat tail artery by neuronal uptake",
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.",
author = "Webb, {R Clinton} and Vanhoutte, {P. M.} and Bohr, {D. F.}",
year = "1980",
month = "1",
day = "1",
doi = "10.1097/00005344-198003000-00004",
language = "English (US)",
volume = "2",
pages = "121--132",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Inactivation of released norepinephrine in rat tail artery by neuronal uptake

AU - Webb, R Clinton

AU - Vanhoutte, P. M.

AU - Bohr, D. F.

PY - 1980/1/1

Y1 - 1980/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0018861443&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018861443&partnerID=8YFLogxK

U2 - 10.1097/00005344-198003000-00004

DO - 10.1097/00005344-198003000-00004

M3 - Article

C2 - 6171680

AN - SCOPUS:0018861443

VL - 2

SP - 121

EP - 132

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 2

ER -