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Article: Vascular actions of TA 3090, a novel analog of diltiazem: Interaction with endothelium-dependent relaxation in canine femoral and coronary arteries

TitleVascular actions of TA 3090, a novel analog of diltiazem: Interaction with endothelium-dependent relaxation in canine femoral and coronary arteries
Authors
Issue Date1991
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, 1991, v. 259 n. 2, p. 639-642 How to Cite?
AbstractThe effects of a new 1,5-benzothiazepine calcium antagonist, TA 3090 (an analog of diltiazem), were analyzed in isolated canine femoral and coronary arteries suspended in organ chambers or studied in a bioassay system. TA 3090 (10 -9 to 10 -4 M) caused comparable relaxations in arterial rings with and without endothelium contracted by prostaglandin F(2α). Coronary arteries were more sensitive to the Ca ++ antagonist. In both preparations, TA 3090 was more potent than diltiazem. In femoral (but not coronary) artery rings with endothelium, acetylcholine (10 -8 M) inhibited relaxations to TA 3090. Previous treatment of femoral or coronary arteries with TA 3090 (10 -6 M) had no effect on endothelium-dependent relaxations to acetylcholine. In a bioassay system, TA 3090 (2 x 10 -7 M) caused partial reversal of acetylcholine-induced relaxation in perfused femoral arteries and superfused coronary arterial rings. The dihydropyridine enantiomer (-)-202,791 did not affect acetylcholine-induced relaxations and did not prevent the reversal by TA 3090. These data indicate that, in addition to a direct action on vascular smooth muscle, this novel benzothiazepine Ca ++-antagonist interferes with the synthesis/release of endothelium-derived relaxing factor stimulated by acetylcholine in canine femoral arteries. These findings, which are similar to those obtained with d-cis-diltiazem, support the hypothesis that a specific benzothiazepine-dependent mechanism(s) can suppress the production of endothelium-derived relaxing factor in endothelial cells.
Persistent Identifierhttp://hdl.handle.net/10722/171041
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRubanyi, Gen_US
dc.contributor.authorIqbal, Aen_US
dc.contributor.authorSchwartz, Aen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:57Z-
dc.date.available2012-10-30T06:11:57Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1991, v. 259 n. 2, p. 639-642en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/171041-
dc.description.abstractThe effects of a new 1,5-benzothiazepine calcium antagonist, TA 3090 (an analog of diltiazem), were analyzed in isolated canine femoral and coronary arteries suspended in organ chambers or studied in a bioassay system. TA 3090 (10 -9 to 10 -4 M) caused comparable relaxations in arterial rings with and without endothelium contracted by prostaglandin F(2α). Coronary arteries were more sensitive to the Ca ++ antagonist. In both preparations, TA 3090 was more potent than diltiazem. In femoral (but not coronary) artery rings with endothelium, acetylcholine (10 -8 M) inhibited relaxations to TA 3090. Previous treatment of femoral or coronary arteries with TA 3090 (10 -6 M) had no effect on endothelium-dependent relaxations to acetylcholine. In a bioassay system, TA 3090 (2 x 10 -7 M) caused partial reversal of acetylcholine-induced relaxation in perfused femoral arteries and superfused coronary arterial rings. The dihydropyridine enantiomer (-)-202,791 did not affect acetylcholine-induced relaxations and did not prevent the reversal by TA 3090. These data indicate that, in addition to a direct action on vascular smooth muscle, this novel benzothiazepine Ca ++-antagonist interferes with the synthesis/release of endothelium-derived relaxing factor stimulated by acetylcholine in canine femoral arteries. These findings, which are similar to those obtained with d-cis-diltiazem, support the hypothesis that a specific benzothiazepine-dependent mechanism(s) can suppress the production of endothelium-derived relaxing factor 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.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshDiltiazem - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFemoral Artery - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.titleVascular actions of TA 3090, a novel analog of diltiazem: Interaction with endothelium-dependent relaxation in canine femoral and coronary 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.pmid1941612-
dc.identifier.scopuseid_2-s2.0-0026345687en_US
dc.identifier.volume259en_US
dc.identifier.issue2en_US
dc.identifier.spage639en_US
dc.identifier.epage642en_US
dc.identifier.isiWOS:A1991GP82300025-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRubanyi, G=7005517991en_US
dc.identifier.scopusauthoridIqbal, A=7005402770en_US
dc.identifier.scopusauthoridSchwartz, A=35227983200en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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