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Article: Potentiation by trandolaprilat of the endothelium-dependent hyperpolarization induced by bradykinin

TitlePotentiation by trandolaprilat of the endothelium-dependent hyperpolarization induced by bradykinin
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. S6-S10 How to Cite?
AbstractIn canine coronary arteries, bradykinin evokes endothelium-dependent relaxations that are mediated by nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). The converting-enzyme inhibitor trandolaprilat potentiates the endothelium-dependent relaxations evoked by bradykinin in this tissue. The present experiments were designed to determine whether or not facilitated release of EDHF contributes to the augmented response to bradykinin in the presence of trandolaprilat. Organ-chamber studies were performed to measure changes in isometric tension in rings of canine coronary arteries. In the presence of nitro-L-arginine, an inhibitor of NO synthase, trandolaprilat augmented the endothelium-dependent relaxations evoked by bradykinin. These relaxations were not inhibited by the K+-channel inhibitors tetraethylammonium, 4-aminopyricine, or glibenclamide, but were abolished in high-potassium solution. The membrane potential in individual smooth-muscle cells of coronary artery was measured by means of glass microelectrodes. Trandolaprilat potentiated the endothelium-dependent hyperpolarizations evoked by a subthreshold concentration of bradykinin, and these endothelium-dependent hyperpolarizations were inhibited by high- potassium solution. These experiments demonstrate that EDHF contributes to the relaxation evoked by bradykinin in the canine coronary artery and that trandolaprilat potentiates the release of this factor. This effect of trandolaprilat may contribute to its vasodilator properties.
Persistent Identifierhttp://hdl.handle.net/10722/171118
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorIlliano, Sen_US
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorNagao, Ten_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:15Z-
dc.date.available2012-10-30T06:12:15Z-
dc.date.issued1994en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1994, v. 23 SUPPL. 4, p. S6-S10en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/171118-
dc.description.abstractIn canine coronary arteries, bradykinin evokes endothelium-dependent relaxations that are mediated by nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). The converting-enzyme inhibitor trandolaprilat potentiates the endothelium-dependent relaxations evoked by bradykinin in this tissue. The present experiments were designed to determine whether or not facilitated release of EDHF contributes to the augmented response to bradykinin in the presence of trandolaprilat. Organ-chamber studies were performed to measure changes in isometric tension in rings of canine coronary arteries. In the presence of nitro-L-arginine, an inhibitor of NO synthase, trandolaprilat augmented the endothelium-dependent relaxations evoked by bradykinin. These relaxations were not inhibited by the K+-channel inhibitors tetraethylammonium, 4-aminopyricine, or glibenclamide, but were abolished in high-potassium solution. The membrane potential in individual smooth-muscle cells of coronary artery was measured by means of glass microelectrodes. Trandolaprilat potentiated the endothelium-dependent hyperpolarizations evoked by a subthreshold concentration of bradykinin, and these endothelium-dependent hyperpolarizations were inhibited by high- potassium solution. These experiments demonstrate that EDHF contributes to the relaxation evoked by bradykinin in the canine coronary artery and that trandolaprilat potentiates the release of this factor. This effect of trandolaprilat may contribute to its vasodilator properties.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.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshBiological Factors - Physiologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshIndoles - Pharmacologyen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshNitroarginineen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titlePotentiation by trandolaprilat of the endothelium-dependent hyperpolarization induced by bradykininen_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.doi10.1097/00005344-199400234-00003-
dc.identifier.pmid7527103-
dc.identifier.scopuseid_2-s2.0-0027935451en_US
dc.identifier.volume23en_US
dc.identifier.issueSUPPL. 4en_US
dc.identifier.spageS6en_US
dc.identifier.epageS10en_US
dc.identifier.isiWOS:A1994PC37800003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridIlliano, S=6602119848en_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridNagao, T=7401489430en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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