File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Inhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veins

TitleInhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veins
Authors
Issue Date1976
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1976, v. 39 n. 2, p. 263-269 How to Cite?
AbstractIn the dog's saphenous vein acetylcholine inhibits the norepinephrine release caused by nerve stimulation, but not that caused by tyramine. Experiments were performed to determine whether acetylcholine affects the release of norepinephrine evoked by high K+ concentrations. The authors recorded changes in isometric tension of dog saphenous vein strips. Acetylcholine (5 x 10-9 to 10-6 g/ml) caused dose dependent relaxations during contractions caused by K+ 40 mEq/liter. These relaxations were not depressed by tetrodotoxin (10-7 g/ml), which abolished the response to nerve stimulation, but were inhibited by atropine (10-7 g/ml). Strips of saphenous veins were incubated with [3H]norepinephrine and mounted for superfusion (3 ml/min) and isometric tension recording; the total radioactivity and the amount of intact [3H]norepinephrine present in the superfusate were determined. K+ at 50 mEq/liter increased tension, total radioactivity of the superfusate, and the [3H]norepinephrine efflux; acetylcholine (10-7 g/ml) depressed the contraction and diminished the efflux of [3H]norepinephrine. Increasing the K+ concentration from 50 to 70 mEq/liter augmented both tension and the evoked release of [3H]norepinephrine. Acetylcholine did not significantly alter the release of [3H]norepinephrine evoked by K+ 120 mEq/liter. These experiments show that acetylcholine inhibits the norepinephrine release evoked by potassium ions, as it does during nerve stimulation. The inhibition of adrenergic neurotransmission is not due to interference with action potential electrogenesis, but probably is caused by hyperpolarization of the adrenergic nerve endings.
Persistent Identifierhttp://hdl.handle.net/10722/170515
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorVerbeuren, TJen_US
dc.date.accessioned2012-10-30T06:09:46Z-
dc.date.available2012-10-30T06:09:46Z-
dc.date.issued1976en_US
dc.identifier.citationCirculation Research, 1976, v. 39 n. 2, p. 263-269en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170515-
dc.description.abstractIn the dog's saphenous vein acetylcholine inhibits the norepinephrine release caused by nerve stimulation, but not that caused by tyramine. Experiments were performed to determine whether acetylcholine affects the release of norepinephrine evoked by high K+ concentrations. The authors recorded changes in isometric tension of dog saphenous vein strips. Acetylcholine (5 x 10-9 to 10-6 g/ml) caused dose dependent relaxations during contractions caused by K+ 40 mEq/liter. These relaxations were not depressed by tetrodotoxin (10-7 g/ml), which abolished the response to nerve stimulation, but were inhibited by atropine (10-7 g/ml). Strips of saphenous veins were incubated with [3H]norepinephrine and mounted for superfusion (3 ml/min) and isometric tension recording; the total radioactivity and the amount of intact [3H]norepinephrine present in the superfusate were determined. K+ at 50 mEq/liter increased tension, total radioactivity of the superfusate, and the [3H]norepinephrine efflux; acetylcholine (10-7 g/ml) depressed the contraction and diminished the efflux of [3H]norepinephrine. Increasing the K+ concentration from 50 to 70 mEq/liter augmented both tension and the evoked release of [3H]norepinephrine. Acetylcholine did not significantly alter the release of [3H]norepinephrine evoked by K+ 120 mEq/liter. These experiments show that acetylcholine inhibits the norepinephrine release evoked by potassium ions, as it does during nerve stimulation. The inhibition of adrenergic neurotransmission is not due to interference with action potential electrogenesis, but probably is caused by hyperpolarization of the adrenergic nerve endings.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.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDepression, Chemicalen_US
dc.subject.meshDogsen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Drug Effectsen_US
dc.subject.meshNorepinephrine - Secretionen_US
dc.subject.meshPhentolamine - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic - Drug Effectsen_US
dc.subject.meshSaphenous Vein - Drug Effects - Innervationen_US
dc.titleInhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veinsen_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.pmid939012-
dc.identifier.scopuseid_2-s2.0-0017148628en_US
dc.identifier.volume39en_US
dc.identifier.issue2en_US
dc.identifier.spage263en_US
dc.identifier.epage269en_US
dc.identifier.isiWOS:A1976CA60600016-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridVerbeuren, TJ=7007006534en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats