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Article: Inhibition by acetylcholine of adrenergic neurotransmission in vascular smooth muscle

TitleInhibition by acetylcholine of adrenergic neurotransmission in vascular smooth muscle
Authors
Issue Date1974
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1974, v. 34 n. 3, p. 317-326 How to Cite?
AbstractChanges in the isometric tension of isolated strips of cutaneous, femoral, mesenteric, pulmonary, and muscle arteries and veins were recorded at 37°C in an organ bath. Acetylcholine (5 x 10-8 and 10-7 g/ml) caused relaxation of strips from the saphenous veins, the femoral veins, and all of the arteries after contraction by norepinephrine released from nerve terminals by electrical stimulation (2-5 Hz); in the pulmonary and mesenteric veins, acetylcholine caused a further increase in tension. Pulmonary artery and mesenteric vein strips were incubated with [3H] norepinephrine and mounted for superfusion (3 ml/min) and isometric tension recording. Electrical stimulation increased the tesion and the total radioactivity released in both preparations. Acetylcholine (2 x 10-7 g/ml) depressed the contractions of the pulmonary artery strips but augmented those of the mesenteric vein strips; it diminished the efflux of radioactivity in both, indicating that acetylcholine inhibits adrenergic neurotransmission. In the absence of sympathetic stimulation, acetylcholine (5 x 10-10-10-5 g/ml) caused all vein strips to contract; the most common reaction in artery strips was a slight relaxation (at 10-9-10-8 g/ml) followed by a contraction (at 5 x 10-8-10-5 g/ml). During contractions caused by norepinephrine, acetylcholine caused a further increase in tension in vein strips but a relaxation in artery strips. Atropine abolished the effects of acetylcholine. The results of this study suggest the presence in vascular smooth muscle of both excitatory and inhibitory cholinergic receptors.
Persistent Identifierhttp://hdl.handle.net/10722/170502
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:09:43Z-
dc.date.available2012-10-30T06:09:43Z-
dc.date.issued1974en_US
dc.identifier.citationCirculation Research, 1974, v. 34 n. 3, p. 317-326en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170502-
dc.description.abstractChanges in the isometric tension of isolated strips of cutaneous, femoral, mesenteric, pulmonary, and muscle arteries and veins were recorded at 37°C in an organ bath. Acetylcholine (5 x 10-8 and 10-7 g/ml) caused relaxation of strips from the saphenous veins, the femoral veins, and all of the arteries after contraction by norepinephrine released from nerve terminals by electrical stimulation (2-5 Hz); in the pulmonary and mesenteric veins, acetylcholine caused a further increase in tension. Pulmonary artery and mesenteric vein strips were incubated with [3H] norepinephrine and mounted for superfusion (3 ml/min) and isometric tension recording. Electrical stimulation increased the tesion and the total radioactivity released in both preparations. Acetylcholine (2 x 10-7 g/ml) depressed the contractions of the pulmonary artery strips but augmented those of the mesenteric vein strips; it diminished the efflux of radioactivity in both, indicating that acetylcholine inhibits adrenergic neurotransmission. In the absence of sympathetic stimulation, acetylcholine (5 x 10-10-10-5 g/ml) caused all vein strips to contract; the most common reaction in artery strips was a slight relaxation (at 10-9-10-8 g/ml) followed by a contraction (at 5 x 10-8-10-5 g/ml). During contractions caused by norepinephrine, acetylcholine caused a further increase in tension in vein strips but a relaxation in artery strips. Atropine abolished the effects of acetylcholine. The results of this study suggest the presence in vascular smooth muscle of both excitatory and inhibitory cholinergic receptors.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.meshAtropine - Pharmacologyen_US
dc.subject.meshBlood Vessels - Innervationen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshFemoral Artery - Innervationen_US
dc.subject.meshFemoral Vein - Innervationen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMesenteric Arteries - Innervationen_US
dc.subject.meshMesenteric Veins - Innervationen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Innervationen_US
dc.subject.meshNorepinephrine - Secretionen_US
dc.subject.meshPulmonary Artery - Innervationen_US
dc.subject.meshPulmonary Veins - Innervationen_US
dc.subject.meshSaphenous Vein - Innervationen_US
dc.subject.meshSynaptic Transmission - Drug Effectsen_US
dc.subject.meshTetrodotoxin - Pharmacologyen_US
dc.subject.meshTibia - Blood Supplyen_US
dc.subject.meshTritiumen_US
dc.subject.meshVasomotor System - Drug Effectsen_US
dc.titleInhibition by acetylcholine of adrenergic neurotransmission in vascular smooth muscleen_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.pmid4362037-
dc.identifier.scopuseid_2-s2.0-0016371915en_US
dc.identifier.volume34en_US
dc.identifier.issue3en_US
dc.identifier.spage317en_US
dc.identifier.epage326en_US
dc.identifier.isiWOS:A1974S731400006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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