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Article: Comparison of the responsiveness of cutaneous veins of dog and rabbit to adrenergic and cholinergic stimulation

TitleComparison of the responsiveness of cutaneous veins of dog and rabbit to adrenergic and cholinergic stimulation
Authors
Issue Date1980
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
Blood Vessels, 1980, v. 17 n. 1, p. 27-43 How to Cite?
AbstractThe reactivity to sympathetic nerve activation and the metabolism of 3H-norepinephrine were compared in isolated saphenous veins of dogs and rabbits. The veins of both species were equally sensitive to electrical stimulation, but the magnitude of the contractile responses to such stimulation was larger in the dog. The response to depolarization of the adrenergic nerve endings by high K+ solutions was depressed by phentolamine to a greater extent in the dog than in the rabbit vein. After incubation with 3H-norepinephrine, electrical stimulation caused a greater evoked release of tritiated transmitter in the dog than in the rabbit veins. These experiments suggest that the former are more densely innervated. In resting conditions and during electrical stimulation, the dog veins and the rabbit veins degraded 3H-norepinephrine in a different way. In both species, neuronal uptake appeared to be of minor importance in the disposition of 3H-norepinephrine released during continuous electrical stimulation. The reactivity to exogenous catecholamines and acetylcholine were also compared in both veins. The apparent sensitivity to exogenous norepinephrine was greater in rabbit than in dog veins. This difference disappeared after inhibition of neuronal uptake with cocaine, suggesting that it is due to the difference in density of adrenergic innervation. There was no interspecies difference in the sensitivity of the β-adrenoceptors, but the maximal effect of β-adrenergic activation by isoproterenol was larger in the dog than in the rabbit veins. In both species acetylcholine caused inhibition of adrenergic neurotransmission, and direct activation of the venous smooth muscle cells. As regards the latter effect, dog veins were less sensitive to acetylcholine but their response was stronger than that of rabbit veins. These results suggest that the density of adrenergic innervation modulates mainly the apparent sensitivity of the venous smooth muscle to α-adrenergic activation.
Persistent Identifierhttp://hdl.handle.net/10722/170602
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDe Mey, JGen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:06Z-
dc.date.available2012-10-30T06:10:06Z-
dc.date.issued1980en_US
dc.identifier.citationBlood Vessels, 1980, v. 17 n. 1, p. 27-43en_US
dc.identifier.issn0303-6847en_US
dc.identifier.urihttp://hdl.handle.net/10722/170602-
dc.description.abstractThe reactivity to sympathetic nerve activation and the metabolism of 3H-norepinephrine were compared in isolated saphenous veins of dogs and rabbits. The veins of both species were equally sensitive to electrical stimulation, but the magnitude of the contractile responses to such stimulation was larger in the dog. The response to depolarization of the adrenergic nerve endings by high K+ solutions was depressed by phentolamine to a greater extent in the dog than in the rabbit vein. After incubation with 3H-norepinephrine, electrical stimulation caused a greater evoked release of tritiated transmitter in the dog than in the rabbit veins. These experiments suggest that the former are more densely innervated. In resting conditions and during electrical stimulation, the dog veins and the rabbit veins degraded 3H-norepinephrine in a different way. In both species, neuronal uptake appeared to be of minor importance in the disposition of 3H-norepinephrine released during continuous electrical stimulation. The reactivity to exogenous catecholamines and acetylcholine were also compared in both veins. The apparent sensitivity to exogenous norepinephrine was greater in rabbit than in dog veins. This difference disappeared after inhibition of neuronal uptake with cocaine, suggesting that it is due to the difference in density of adrenergic innervation. There was no interspecies difference in the sensitivity of the β-adrenoceptors, but the maximal effect of β-adrenergic activation by isoproterenol was larger in the dog than in the rabbit veins. In both species acetylcholine caused inhibition of adrenergic neurotransmission, and direct activation of the venous smooth muscle cells. As regards the latter effect, dog veins were less sensitive to acetylcholine but their response was stronger than that of rabbit veins. These results suggest that the density of adrenergic innervation modulates mainly the apparent sensitivity of the venous smooth muscle to α-adrenergic activation.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVRen_US
dc.relation.ispartofBlood Vesselsen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCocaine - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMandelic Acids - Pharmacologyen_US
dc.subject.meshMethoxyhydroxyphenylglycol - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshParasympathetic Nervous System - Physiologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshPyrogallol - Pharmacologyen_US
dc.subject.meshRabbitsen_US
dc.subject.meshSaphenous Vein - Physiologyen_US
dc.subject.meshSkin - Blood Supplyen_US
dc.subject.meshSpecies Specificityen_US
dc.subject.meshSympathetic Nervous System - Physiologyen_US
dc.subject.meshVanilmandelic Acid - Pharmacologyen_US
dc.titleComparison of the responsiveness of cutaneous veins of dog and rabbit to adrenergic and cholinergic stimulationen_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.pmid7357094en_US
dc.identifier.scopuseid_2-s2.0-0018873704en_US
dc.identifier.volume17en_US
dc.identifier.issue1en_US
dc.identifier.spage27en_US
dc.identifier.epage43en_US
dc.identifier.isiWOS:A1980JM81200003-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridDe Mey, JG=7101918486en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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