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- Publisher Website: 10.1161/01.RES.39.2.263
- Scopus: eid_2-s2.0-0017148628
- PMID: 939012
- WOS: WOS:A1976CA60600016
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Article: Inhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veins
Title | Inhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veins |
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Authors | |
Issue Date | 1976 |
Publisher | Lippincott 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? |
Abstract | In 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 Identifier | http://hdl.handle.net/10722/170515 |
ISSN | 2023 Impact Factor: 16.5 2023 SCImago Journal Rankings: 4.903 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Vanhoutte, PM | en_US |
dc.contributor.author | Verbeuren, TJ | en_US |
dc.date.accessioned | 2012-10-30T06:09:46Z | - |
dc.date.available | 2012-10-30T06:09:46Z | - |
dc.date.issued | 1976 | en_US |
dc.identifier.citation | Circulation Research, 1976, v. 39 n. 2, p. 263-269 | en_US |
dc.identifier.issn | 0009-7330 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170515 | - |
dc.description.abstract | In 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.language | eng | en_US |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org | en_US |
dc.relation.ispartof | Circulation Research | en_US |
dc.subject.mesh | Acetylcholine - Pharmacology | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Depression, Chemical | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Muscle Contraction - Drug Effects | en_US |
dc.subject.mesh | Muscle, Smooth - Drug Effects | en_US |
dc.subject.mesh | Norepinephrine - Secretion | en_US |
dc.subject.mesh | Phentolamine - Pharmacology | en_US |
dc.subject.mesh | Potassium - Pharmacology | en_US |
dc.subject.mesh | Receptors, Adrenergic - Drug Effects | en_US |
dc.subject.mesh | Saphenous Vein - Drug Effects - Innervation | en_US |
dc.title | Inhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veins | 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 | 10.1161/01.RES.39.2.263 | - |
dc.identifier.pmid | 939012 | - |
dc.identifier.scopus | eid_2-s2.0-0017148628 | en_US |
dc.identifier.volume | 39 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 263 | en_US |
dc.identifier.epage | 269 | en_US |
dc.identifier.isi | WOS:A1976CA60600016 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.scopusauthorid | Verbeuren, TJ=7007006534 | en_US |
dc.identifier.issnl | 0009-7330 | - |