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Article: Effects of buflomedil on the responsiveness of canine vascular smooth muscle

TitleEffects of buflomedil on the responsiveness of canine vascular smooth muscle
Authors
Issue Date1983
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, 1983, v. 227 n. 3, p. 613-620 How to Cite?
AbstractExperiments were designed to determine the effect of buflomedil on vascular responsiveness. Rings of canine arteries and veins were suspended for isometric tension recording at 37° C. Buflomedil caused concentration-dependent inhibition of the contractile responses to norepinephrine, methoxamine, phenylephrine, clonidine, xylazine and sympathetic nerve activation, but not of the responses to potassium, prostaglandin F(2α), acetylcholine or 5-hydroxytryptamine. The inhibitory effect of buflomedil was not afffected by endothelium removal but was reduced by chemical sympathectomy with 6-hydroxydopamine and by inhibitors of neuronal uptake. Strips of canine saphenous veins were superfused after incubation with [3H]norepinephrine. Buflomedil augmented the efflux of [3H]norepinephrine, 3,4-[3H]dihydroxyphenylglycol, 3,4-[3H]dihydroxymandelic acid and [3H]-3-methoxy-4-hydroxyphenylglycol under basal conditions and the overflow of [3H]norepinephrine, 3,4-[3H]dihydroxymandelic acid and 3,4-[3H]dihydroxyphenylglycol during sympathetic nerve activation. The augmentation by buflomedil of the release of [3H]norepinephrine evoked by electrical stimulation was prevented by phentolamine. In the perfused gracilis muscle of the anesthetized dog, buflomedil depressed the vasoconstrictor response to norepinephrine more than that evoked by angiotensin II. These experiments suggest that buflomedil blocks alpha adrenoceptors, but is not selective for either the alpha-1 or alpha-2 adrenoceptor subtype. The presence of adrenergic nerve endings appear to augment the postjunctional inhibitory effects of buflomedil.
Persistent Identifierhttp://hdl.handle.net/10722/170712
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorAarhus, LLen_US
dc.contributor.authorCoen, Een_US
dc.date.accessioned2012-10-30T06:10:33Z-
dc.date.available2012-10-30T06:10:33Z-
dc.date.issued1983en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1983, v. 227 n. 3, p. 613-620en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170712-
dc.description.abstractExperiments were designed to determine the effect of buflomedil on vascular responsiveness. Rings of canine arteries and veins were suspended for isometric tension recording at 37° C. Buflomedil caused concentration-dependent inhibition of the contractile responses to norepinephrine, methoxamine, phenylephrine, clonidine, xylazine and sympathetic nerve activation, but not of the responses to potassium, prostaglandin F(2α), acetylcholine or 5-hydroxytryptamine. The inhibitory effect of buflomedil was not afffected by endothelium removal but was reduced by chemical sympathectomy with 6-hydroxydopamine and by inhibitors of neuronal uptake. Strips of canine saphenous veins were superfused after incubation with [3H]norepinephrine. Buflomedil augmented the efflux of [3H]norepinephrine, 3,4-[3H]dihydroxyphenylglycol, 3,4-[3H]dihydroxymandelic acid and [3H]-3-methoxy-4-hydroxyphenylglycol under basal conditions and the overflow of [3H]norepinephrine, 3,4-[3H]dihydroxymandelic acid and 3,4-[3H]dihydroxyphenylglycol during sympathetic nerve activation. The augmentation by buflomedil of the release of [3H]norepinephrine evoked by electrical stimulation was prevented by phentolamine. In the perfused gracilis muscle of the anesthetized dog, buflomedil depressed the vasoconstrictor response to norepinephrine more than that evoked by angiotensin II. These experiments suggest that buflomedil blocks alpha adrenoceptors, but is not selective for either the alpha-1 or alpha-2 adrenoceptor subtype. The presence of adrenergic nerve endings appear to augment the postjunctional inhibitory effects of buflomedil.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-Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshEndothelium - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHydroxydopaminesen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshOxidopamineen_US
dc.subject.meshPyrrolidines - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Drug Effectsen_US
dc.subject.meshSympathectomy, Chemicalen_US
dc.subject.meshVasoconstrictor Agents - Antagonists & Inhibitorsen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleEffects of buflomedil on the responsiveness of canine 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.pmid6140306-
dc.identifier.scopuseid_2-s2.0-0021020523en_US
dc.identifier.volume227en_US
dc.identifier.issue3en_US
dc.identifier.spage613en_US
dc.identifier.epage620en_US
dc.identifier.isiWOS:A1983RV32700011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridAarhus, LL=7003305335en_US
dc.identifier.scopusauthoridCoen, E=35501191200en_US

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