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Article: Endothelium-dependent inhibitory effect of acetylcholine, adenosine triphosphate, thrombin and arachidonic acid in the canine femoral artery

TitleEndothelium-dependent inhibitory effect of acetylcholine, adenosine triphosphate, thrombin and arachidonic acid in the canine femoral artery
Authors
Issue Date1982
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, 1982, v. 222 n. 1, p. 166-173 How to Cite?
AbstractExperiments were designed to investigate the importance of endothelial metabolism or arachidonic acid in the relaxation of isolated arteries caused by acetylcholine, ATP, arachidonic acid itself and thrombin. Rings of canine femoral arteries were mounted for isometric tension recording in organ chambers filled with Krebs-Ringer-bicarbonate solution. Acetylcholine, arachidonic acid, ATP, 15-hydroperoxy-5,8,11,13 eicosatetraenoic acid, thrombin and prostacyclin caused relaxations of control rings made to contract with norepinephrine. Removal of the endothelium abolished the relaxation caused by acetylcholine, ATP, thrombin and 15-hydroperoxy-5,8,11,13 eicosatetraenoic acid, reduced those caused by arachidonic acid, but did not affect the inhibitory effect of prostacyclin. The inhibitory response to arachidonic acid was abolished by indomethacin and 5,8,11,14-eicosatetraynoic acid (ETYA); that to acetylcholine was abolished by mepacrine and reduced by ETYA. The relaxations induced by thrombin and ATP were not affected by these inhibitors. Canine femoral arteries with endothelium, but not de-endothelialized preparations, transformed part of exogenously added [14C]arachidonic acid to prostaglandins (6-oxo-prostaglandin (F(1α)) and a hydroxy derivative. The formation of prostanoids was inhibited by indomethacin, ETYA and 15-hydroperoxy-5,8,11,13 eicosatetraenoic acid and that of hydroxy derivative by ETYA. These results suggest that the endothelial cells of canine femoral arteries initiate relaxation of the vascular smooth muscle cells of the media by: (1) producing prostacyclin, when exposed to arachidonic acid; (2) producing a lipoxygenase product, when exposed to acetylcholine; and (3) producing a signal of unknown nature, when exposed to thrombin or ATP.
Persistent Identifierhttp://hdl.handle.net/10722/170666
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDe Mey, JGen_US
dc.contributor.authorClaeys, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:20Z-
dc.date.available2012-10-30T06:10:20Z-
dc.date.issued1982en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1982, v. 222 n. 1, p. 166-173en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170666-
dc.description.abstractExperiments were designed to investigate the importance of endothelial metabolism or arachidonic acid in the relaxation of isolated arteries caused by acetylcholine, ATP, arachidonic acid itself and thrombin. Rings of canine femoral arteries were mounted for isometric tension recording in organ chambers filled with Krebs-Ringer-bicarbonate solution. Acetylcholine, arachidonic acid, ATP, 15-hydroperoxy-5,8,11,13 eicosatetraenoic acid, thrombin and prostacyclin caused relaxations of control rings made to contract with norepinephrine. Removal of the endothelium abolished the relaxation caused by acetylcholine, ATP, thrombin and 15-hydroperoxy-5,8,11,13 eicosatetraenoic acid, reduced those caused by arachidonic acid, but did not affect the inhibitory effect of prostacyclin. The inhibitory response to arachidonic acid was abolished by indomethacin and 5,8,11,14-eicosatetraynoic acid (ETYA); that to acetylcholine was abolished by mepacrine and reduced by ETYA. The relaxations induced by thrombin and ATP were not affected by these inhibitors. Canine femoral arteries with endothelium, but not de-endothelialized preparations, transformed part of exogenously added [14C]arachidonic acid to prostaglandins (6-oxo-prostaglandin (F(1α)) and a hydroxy derivative. The formation of prostanoids was inhibited by indomethacin, ETYA and 15-hydroperoxy-5,8,11,13 eicosatetraenoic acid and that of hydroxy derivative by ETYA. These results suggest that the endothelial cells of canine femoral arteries initiate relaxation of the vascular smooth muscle cells of the media by: (1) producing prostacyclin, when exposed to arachidonic acid; (2) producing a lipoxygenase product, when exposed to acetylcholine; and (3) producing a signal of unknown nature, when exposed to thrombin or ATP.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.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdenosine Triphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArachidonic Aciden_US
dc.subject.meshArachidonic Acids - Pharmacologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium - Cytology - Physiologyen_US
dc.subject.meshFemoral Artery - Drug Effectsen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshThrombin - Pharmacologyen_US
dc.titleEndothelium-dependent inhibitory effect of acetylcholine, adenosine triphosphate, thrombin and arachidonic acid in the canine femoral arteryen_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.pmid6806467-
dc.identifier.scopuseid_2-s2.0-0019979079en_US
dc.identifier.volume222en_US
dc.identifier.issue1en_US
dc.identifier.spage166en_US
dc.identifier.epage173en_US
dc.identifier.isiWOS:A1982NY10400026-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDe Mey, JG=7101918486en_US
dc.identifier.scopusauthoridClaeys, M=7102514911en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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