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Article: Electrophysiological analysis of adrenergic neurotransmission and its modulation by chronic denervation in canine saphenous veins

TitleElectrophysiological analysis of adrenergic neurotransmission and its modulation by chronic denervation in canine saphenous veins
Authors
Issue Date1990
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 1990, v. 252 n. 3, p. 1197-1201 How to Cite?
AbstractThe present experiments were undertaken to investigate the electrophysiological responses of the canine saphenous vein evoked by perivascular nerve stimulation, norepinephrine or selective alpha adrenergic agonists before and after chronic sympathetic denervation. Unilateral sympathectomy was performed from T12 to L9 in adult female dogs. After 3 to 5 weeks, the denervated saphenous veins were removed. Innervated saphenous veins were obtained from unoperated dogs. In innervated but not in denervated veins, electrical stimulation generated excitatory junction potentials and a slow depolarization. The slow depolarization was inhibited by rauwolescine or phentolamine, but not by prazosin, whereas excitatory junction potentials were not inhibited by alpha adrenergic blockers. Exogenously applied norepinephrine caused a depolarization of the membrane that was inhibited by rauwolscine but not by prazosin. The selective alpha-1 adrenergic agonist, phenylephrine, and the selective alpha-2 adrenergic agonist, UK 14,304, caused depolarization. In denervated veins, the threshold concentrations of norepinephrine or UK 14,304 required to depolarize the smooth muscle cell membrane were reduced. Responses to phenylephrine were not affected by denervation. These results indicate that in the canine saphenous vein norepinephrine, whether added exogenously or released from sympathetic nerves, causes predominant depolarization by activating alpha-2 adrenergic receptors. Denervation augments selectively the electrical response to alpha-2 adrenergic stimulation.
Persistent Identifierhttp://hdl.handle.net/10722/170982
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847

 

DC FieldValueLanguage
dc.contributor.authorKomori, Ken_US
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorMiller, VMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:42Z-
dc.date.available2012-10-30T06:11:42Z-
dc.date.issued1990en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1990, v. 252 n. 3, p. 1197-1201en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170982-
dc.description.abstractThe present experiments were undertaken to investigate the electrophysiological responses of the canine saphenous vein evoked by perivascular nerve stimulation, norepinephrine or selective alpha adrenergic agonists before and after chronic sympathetic denervation. Unilateral sympathectomy was performed from T12 to L9 in adult female dogs. After 3 to 5 weeks, the denervated saphenous veins were removed. Innervated saphenous veins were obtained from unoperated dogs. In innervated but not in denervated veins, electrical stimulation generated excitatory junction potentials and a slow depolarization. The slow depolarization was inhibited by rauwolescine or phentolamine, but not by prazosin, whereas excitatory junction potentials were not inhibited by alpha adrenergic blockers. Exogenously applied norepinephrine caused a depolarization of the membrane that was inhibited by rauwolscine but not by prazosin. The selective alpha-1 adrenergic agonist, phenylephrine, and the selective alpha-2 adrenergic agonist, UK 14,304, caused depolarization. In denervated veins, the threshold concentrations of norepinephrine or UK 14,304 required to depolarize the smooth muscle cell membrane were reduced. Responses to phenylephrine were not affected by denervation. These results indicate that in the canine saphenous vein norepinephrine, whether added exogenously or released from sympathetic nerves, causes predominant depolarization by activating alpha-2 adrenergic receptors. Denervation augments selectively the electrical response to alpha-2 adrenergic stimulation.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_US
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_US
dc.subject.meshAdrenergic Alpha-Agonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMuscle Denervationen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshNeuromuscular Junction - Drug Effectsen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPrazosin - Pharmacologyen_US
dc.subject.meshQuinoxalines - Pharmacologyen_US
dc.subject.meshSaphenous Veinen_US
dc.subject.meshSynaptic Transmission - Drug Effectsen_US
dc.titleElectrophysiological analysis of adrenergic neurotransmission and its modulation by chronic denervation 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.pmid1969471-
dc.identifier.scopuseid_2-s2.0-0025230795en_US
dc.identifier.volume252en_US
dc.identifier.issue3en_US
dc.identifier.spage1197en_US
dc.identifier.epage1201en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKomori, K=8977740100en_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridMiller, VM=7201476816en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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