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Article: Stereoselective effect of diltiazem on endothelium-dependent relaxations in canine femoral arteries

TitleStereoselective effect of diltiazem on endothelium-dependent relaxations in canine femoral arteries
Authors
Issue Date1988
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, 1988, v. 246 n. 1, p. 60-64 How to Cite?
AbstractExperiments were designed to analyze potential interactions between voltage-dependent calcium channel blockers and endothelium-dependent vascular responses. Rings of canine femoral artery were suspended for isometric force recording in organ chambers and contracted with prostaglandin F(2α). Removal of the endothelium had no effect on relaxations induced by d-cis-diltiazem (active stereoisomer), verapamil or nimodipine. When rings with endothelium were first partially relaxed with acetylcholine or the calcium ionophore A23187 the concentration-relaxation curve to d-cis-diltiazem (but not to verapamil or nimodipine) was significantly shifted to the right. Partial relaxation of femoral arterial rings without endothelium by sodium nitroprusside had no effect on relaxations evoked by diltiazem. Pretreatment with diltiazem (10 -6 M) had no effect on endothelium-dependent relaxations to acetylcholine in femoral artery rings. D-cis-Diltiazem partially reversed the relaxation induced by acetylcholine in a bioassay system, in which a ring of canine coronary artery without endothelium was superfused by solution passing through a segment of femoral artery with endothelium. D-cis-Diltiazem relaxed the bioassay ring when infused downstream of the perfused femoral artery with, or upstream of a femoral artery without endothelium. The effect of diltiazem was stereoselective (the less active 1-cis-diltiazem had no effect). Verapamil did not reverse the relaxation induced by acetylcholine and did not affect the reversal induced by diltiazem. These findings indicate that diltiazem specifically antagonizes the production and/or the release of endothelium-derived relaxing factor(s) stimulated by acetylcholine or A23187 in canine femoral arteries. The mechanism involves either a specific benzothiazepine-dependent inhibition of calcium influx or an interference with some other calcium-dependent or independent process in endothelial cells.
Persistent Identifierhttp://hdl.handle.net/10722/170874
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRubanyi, GMen_US
dc.contributor.authorHoeffner, Uen_US
dc.contributor.authorSchwartz, Aen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:13Z-
dc.date.available2012-10-30T06:11:13Z-
dc.date.issued1988en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1988, v. 246 n. 1, p. 60-64en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170874-
dc.description.abstractExperiments were designed to analyze potential interactions between voltage-dependent calcium channel blockers and endothelium-dependent vascular responses. Rings of canine femoral artery were suspended for isometric force recording in organ chambers and contracted with prostaglandin F(2α). Removal of the endothelium had no effect on relaxations induced by d-cis-diltiazem (active stereoisomer), verapamil or nimodipine. When rings with endothelium were first partially relaxed with acetylcholine or the calcium ionophore A23187 the concentration-relaxation curve to d-cis-diltiazem (but not to verapamil or nimodipine) was significantly shifted to the right. Partial relaxation of femoral arterial rings without endothelium by sodium nitroprusside had no effect on relaxations evoked by diltiazem. Pretreatment with diltiazem (10 -6 M) had no effect on endothelium-dependent relaxations to acetylcholine in femoral artery rings. D-cis-Diltiazem partially reversed the relaxation induced by acetylcholine in a bioassay system, in which a ring of canine coronary artery without endothelium was superfused by solution passing through a segment of femoral artery with endothelium. D-cis-Diltiazem relaxed the bioassay ring when infused downstream of the perfused femoral artery with, or upstream of a femoral artery without endothelium. The effect of diltiazem was stereoselective (the less active 1-cis-diltiazem had no effect). Verapamil did not reverse the relaxation induced by acetylcholine and did not affect the reversal induced by diltiazem. These findings indicate that diltiazem specifically antagonizes the production and/or the release of endothelium-derived relaxing factor(s) stimulated by acetylcholine or A23187 in canine femoral arteries. The mechanism involves either a specific benzothiazepine-dependent inhibition of calcium influx or an interference with some other calcium-dependent or independent process in endothelial cells.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.meshBiological Agents - Metabolismen_US
dc.subject.meshBiological Assayen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshDiltiazem - Pharmacologyen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshFemoral Artery - Drug Effects - Metabolismen_US
dc.subject.meshIon Channels - Drug Effects - Metabolismen_US
dc.subject.meshNitric Oxideen_US
dc.subject.meshProstaglandins F - Pharmacologyen_US
dc.subject.meshStereoisomerismen_US
dc.subject.meshVasodilationen_US
dc.titleStereoselective effect of diltiazem on endothelium-dependent relaxations in canine femoral arteriesen_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.pmid2455796-
dc.identifier.scopuseid_2-s2.0-0023747199en_US
dc.identifier.volume246en_US
dc.identifier.issue1en_US
dc.identifier.spage60en_US
dc.identifier.epage64en_US
dc.identifier.isiWOS:A1988P237700009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRubanyi, GM=7005517991en_US
dc.identifier.scopusauthoridHoeffner, U=7801661618en_US
dc.identifier.scopusauthoridSchwartz, A=35227983200en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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