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Article: Inhibitory effect of lidoflazine on contractions of isolated canine coronary arteries caused by norepinephrine, 5-hydroxytryptamine, high potassium, anoxia and ergonovine maleate

TitleInhibitory effect of lidoflazine on contractions of isolated canine coronary arteries caused by norepinephrine, 5-hydroxytryptamine, high potassium, anoxia and ergonovine maleate
Authors
Issue Date1980
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, 1980, v. 213 n. 1, p. 179-187 How to Cite?
AbstractExperiments were performed on isolated coronary arteries to determine whether or not lidoflazine, an agent reported to be beneficial in the treatment of angina pectoris, is effective in antagonizing coronary vasoconstriction. Segments of canine circumflex and right coronary arteries were suspended in organ chambers filled with aerated Krebs-Henseleit solution (37°C) for continuous isometric tension recordings. Dose-dependent contractions were obtained with norepinephrine (in presence of propranolol) and 5-hydroxytryptamine; these contractile responses were antagonized by phentolamine and methysergide, respectively. Lidoflazine caused long-lasting, and dose-dependent inhibition of the responses to both norepinephrine and 5-hydroxytryptamine. High K+ solution (30 mM) caused sustained contraction of the coronary segments; these responses were depressed in a dose-dependent manner by lidoflazine. Lidoflazine slightly augmented relaxations caused by adenosine. Addition of Ca++ to the bath solution partially reversed the inhibitory effect of lidoflazine, which indicates that the compounds acts by inhibiting the influx of extracellular Ca++. Segments incubated in solution containing 20 mM K+ and subjected to anoxia exhibited transient contractions which were inhibited by lidoflazine. Ergonovine maleate caused contractures of the coronary arteries which also were antagonized in a dose-dependent manner by lidoflazine. These experiments demonstrate the ability of lidoflazine to counteract contractions of coronary vascular smooth muscle caused by factors which may be involved in the etiology of coronary vasospasm.
Persistent Identifierhttp://hdl.handle.net/10722/170597
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVan Nuete, JMen_US
dc.contributor.authorVan Beek, Jen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:05Z-
dc.date.available2012-10-30T06:10:05Z-
dc.date.issued1980en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1980, v. 213 n. 1, p. 179-187en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170597-
dc.description.abstractExperiments were performed on isolated coronary arteries to determine whether or not lidoflazine, an agent reported to be beneficial in the treatment of angina pectoris, is effective in antagonizing coronary vasoconstriction. Segments of canine circumflex and right coronary arteries were suspended in organ chambers filled with aerated Krebs-Henseleit solution (37°C) for continuous isometric tension recordings. Dose-dependent contractions were obtained with norepinephrine (in presence of propranolol) and 5-hydroxytryptamine; these contractile responses were antagonized by phentolamine and methysergide, respectively. Lidoflazine caused long-lasting, and dose-dependent inhibition of the responses to both norepinephrine and 5-hydroxytryptamine. High K+ solution (30 mM) caused sustained contraction of the coronary segments; these responses were depressed in a dose-dependent manner by lidoflazine. Lidoflazine slightly augmented relaxations caused by adenosine. Addition of Ca++ to the bath solution partially reversed the inhibitory effect of lidoflazine, which indicates that the compounds acts by inhibiting the influx of extracellular Ca++. Segments incubated in solution containing 20 mM K+ and subjected to anoxia exhibited transient contractions which were inhibited by lidoflazine. Ergonovine maleate caused contractures of the coronary arteries which also were antagonized in a dose-dependent manner by lidoflazine. These experiments demonstrate the ability of lidoflazine to counteract contractions of coronary vascular smooth muscle caused by factors which may be involved in the etiology of coronary vasospasm.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.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshDogsen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshErgonovine - Pharmacologyen_US
dc.subject.meshLidoflazine - Pharmacologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshOxygen - Pharmacologyen_US
dc.subject.meshPiperazines - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleInhibitory effect of lidoflazine on contractions of isolated canine coronary arteries caused by norepinephrine, 5-hydroxytryptamine, high potassium, anoxia and ergonovine maleateen_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.pmid7359366en_US
dc.identifier.scopuseid_2-s2.0-0018822420en_US
dc.identifier.volume213en_US
dc.identifier.issue1en_US
dc.identifier.spage179en_US
dc.identifier.epage187en_US
dc.identifier.isiWOS:A1980JM98000032-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVan Nuete, JM=6503978835en_US
dc.identifier.scopusauthoridVan Beek, J=7005937094en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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