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Article: Endothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries

TitleEndothelium-dependent hyperpolarization caused by bradykinin in human coronary arteries
Authors
Issue Date1993
PublisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.org
Citation
Journal Of Clinical Investigation, 1993, v. 92 n. 6, p. 2867-2871 How to Cite?
AbstractThe present study was designed to determine whether bradykinin induces endothelium-dependent hyperpolarization of vascular smooth muscle in human coronary arteries, and if so, to define the contribution of this hyperpolarization to endothelium-dependent relaxations. The membrane potential of arterial smooth muscle cells (measured by glass microelectrodes) and changes in isometric force were recorded in tissues from six patients undergoing heart transplantation. In the presence of indomethacin and N(G)- nitro-L-arginine (NLA), the membrane potential was -48.3±0.6 and -46.9±0.6 mV, in preparations with and without endothelium, respectively, and was not affected by treatment with perindoprilat, an angiotensin-converting enzyme inhibitor. In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187. Glibenclamide did not inhibit membrane hyperpolarization to bradykinin. In rings contracted with prostaglandin F(2α), the cumulative addition of bradykinin caused a concentration- dependent relaxation during contractions evoked by prostaglandin F(2α), which was not abolished by NLA and indomethacin. The present findings demonstrate the occurrence of endothelium-dependent hyperpolarization, and its contribution to endothelium-dependent relaxations, in the human coronary artery.
Persistent Identifierhttp://hdl.handle.net/10722/171080
ISSN
2015 Impact Factor: 12.575
2015 SCImago Journal Rankings: 8.764
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNakashima, Men_US
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorTaylor, AAen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:07Z-
dc.date.available2012-10-30T06:12:07Z-
dc.date.issued1993en_US
dc.identifier.citationJournal Of Clinical Investigation, 1993, v. 92 n. 6, p. 2867-2871en_US
dc.identifier.issn0021-9738en_US
dc.identifier.urihttp://hdl.handle.net/10722/171080-
dc.description.abstractThe present study was designed to determine whether bradykinin induces endothelium-dependent hyperpolarization of vascular smooth muscle in human coronary arteries, and if so, to define the contribution of this hyperpolarization to endothelium-dependent relaxations. The membrane potential of arterial smooth muscle cells (measured by glass microelectrodes) and changes in isometric force were recorded in tissues from six patients undergoing heart transplantation. In the presence of indomethacin and N(G)- nitro-L-arginine (NLA), the membrane potential was -48.3±0.6 and -46.9±0.6 mV, in preparations with and without endothelium, respectively, and was not affected by treatment with perindoprilat, an angiotensin-converting enzyme inhibitor. In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187. Glibenclamide did not inhibit membrane hyperpolarization to bradykinin. In rings contracted with prostaglandin F(2α), the cumulative addition of bradykinin caused a concentration- dependent relaxation during contractions evoked by prostaglandin F(2α), which was not abolished by NLA and indomethacin. The present findings demonstrate the occurrence of endothelium-dependent hyperpolarization, and its contribution to endothelium-dependent relaxations, in the human coronary artery.en_US
dc.languageengen_US
dc.publisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.orgen_US
dc.relation.ispartofJournal of Clinical Investigationen_US
dc.subject.meshAgeden_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshBenzopyrans - Pharmacologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshChilden_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiology - Physiopathologyen_US
dc.subject.meshCromakalimen_US
dc.subject.meshDinoprost - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Physiology - Physiopathologyen_US
dc.subject.meshGlyburide - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshIndoles - Pharmacologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshInfanten_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiology - Physiopathologyen_US
dc.subject.meshNitroarginineen_US
dc.subject.meshPyrroles - Pharmacologyen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleEndothelium-dependent hyperpolarization caused by bradykinin in human 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.doi10.1172/JCI116907-
dc.identifier.pmid8254041-
dc.identifier.scopuseid_2-s2.0-0027132065en_US
dc.identifier.volume92en_US
dc.identifier.issue6en_US
dc.identifier.spage2867en_US
dc.identifier.epage2871en_US
dc.identifier.isiWOS:A1993ML64300042-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNakashima, M=35599797500en_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridTaylor, AA=8157815100en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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