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Article: The endothelium and vascular effects of the ACE inhibitor trandolaprilat

TitleThe endothelium and vascular effects of the ACE inhibitor trandolaprilat
Authors
Issue Date1994
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1994, v. 23 SUPPL. 4, p. S1-S5 How to Cite?
AbstractExperiments were designed to study the effects of trandolaprilat on endothelium-dependent responses in isolated blood vessels. Rings of either femoral or left circumflex coronary arteries of the dog or thoracic aortas of normotensive rats were suspended in organ chambers for isometric tension recording. During contractions induced by prostaglandin F(2α), trandolaprilat did not cause direct endothelium-dependent or independent relaxation. However, when given to preparations incubated with angiotensin I or bradykinin, the compound evoked significant endothelium-dependent relaxation. By contrast, trandolaprilat failed to cause any change in tension when given in the presence of acetylcholine (ACh). In rings of femoral arteries, trandolaprilat potentiated the endothelium-dependent relaxation evoked by bradykinin and adenosine diphosphate: it did not modify the endothelium-dependent relaxations, induced by ACh, substance P, or thrombin. In rings of femoral arteries without endothelium, trandolaprilat augmented relaxation induced by adenosine diphosphate (ADP) but not by adenosine. In perfused coronary arteries with but not those without endothelium, trandolaprilat caused relaxation in the absence of exogenous bradykinin (or ADP). These experiments suggest that trandolaprilat does not directly release endothelium-derived relaxing factor from the endothelial cells, does not interfere with the ability of the endothelium to release endothelium-derived relaxing factor, augments the endothelium-dependent responses to bradykinin (given exogenously or produced locally) and angiotensin I by direct interaction with converting enzyme, and potentiates the relaxation induced by ADP by augmenting its direct effect on vascular smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/171122
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVidal, Men_US
dc.contributor.authorJoly, Gen_US
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorBoulanger, CMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:17Z-
dc.date.available2012-10-30T06:12:17Z-
dc.date.issued1994en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1994, v. 23 SUPPL. 4, p. S1-S5en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/171122-
dc.description.abstractExperiments were designed to study the effects of trandolaprilat on endothelium-dependent responses in isolated blood vessels. Rings of either femoral or left circumflex coronary arteries of the dog or thoracic aortas of normotensive rats were suspended in organ chambers for isometric tension recording. During contractions induced by prostaglandin F(2α), trandolaprilat did not cause direct endothelium-dependent or independent relaxation. However, when given to preparations incubated with angiotensin I or bradykinin, the compound evoked significant endothelium-dependent relaxation. By contrast, trandolaprilat failed to cause any change in tension when given in the presence of acetylcholine (ACh). In rings of femoral arteries, trandolaprilat potentiated the endothelium-dependent relaxation evoked by bradykinin and adenosine diphosphate: it did not modify the endothelium-dependent relaxations, induced by ACh, substance P, or thrombin. In rings of femoral arteries without endothelium, trandolaprilat augmented relaxation induced by adenosine diphosphate (ADP) but not by adenosine. In perfused coronary arteries with but not those without endothelium, trandolaprilat caused relaxation in the absence of exogenous bradykinin (or ADP). These experiments suggest that trandolaprilat does not directly release endothelium-derived relaxing factor from the endothelial cells, does not interfere with the ability of the endothelium to release endothelium-derived relaxing factor, augments the endothelium-dependent responses to bradykinin (given exogenously or produced locally) and angiotensin I by direct interaction with converting enzyme, and potentiates the relaxation induced by ADP by augmenting its direct effect on vascular smooth muscle.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAdenosine Diphosphate - Pharmacologyen_US
dc.subject.meshAngiotensin I - Pharmacologyen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshIndoles - Pharmacologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleThe endothelium and vascular effects of the ACE inhibitor trandolaprilaten_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.doi10.1097/00005344-199400234-00002-
dc.identifier.pmid7527094-
dc.identifier.scopuseid_2-s2.0-0028017666en_US
dc.identifier.volume23en_US
dc.identifier.issueSUPPL. 4en_US
dc.identifier.spageS1en_US
dc.identifier.epageS5en_US
dc.identifier.isiWOS:A1994PC37800002-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVidal, M=7202764932en_US
dc.identifier.scopusauthoridJoly, G=7005110329en_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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