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Article: Calmodulin antagonists inhibit endothelium-dependent hyperpolarization in the canine coronary artery

TitleCalmodulin antagonists inhibit endothelium-dependent hyperpolarization in the canine coronary artery
Authors
Issue Date1992
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 1992, v. 107 n. 2, p. 382-386 How to Cite?
Abstract1. The effects of the calmodulin antagonists, calmidazolium and fendiline were investigated on endothelium-dependent hyperpolarization in the canine coronary artery. The membrane potential of vascular smooth muscle cells was measured with the microelectrode technique. 2. Smooth muscle cells of the canine coronary artery had a resting membrane potential of -50 mV. Bradykinin and the Ca2+-ionophore, A23187, induced concentration- and endothelium-dependent hyperpolarization. The hyperpolarization induced by a supramaximal concentration of bradykinin (10-6 M) reached approximately 20 mV. 3. Calmidazolium (10-5 M) and fendiline (10-4 M) inhibited hyperpolarization induced by bradykinin and A23187. By contrast, calmidazolium did not affect the hyperpolarization induced by lemakalim, an opener of ATP-sensitive K+-channels. 4. These observations suggest that calmodulin is involved in the generation of endothelium-dependent membrane hyperpolarization of vascular smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/171073
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNagao, Ten_US
dc.contributor.authorIlliano, Sen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:05Z-
dc.date.available2012-10-30T06:12:05Z-
dc.date.issued1992en_US
dc.identifier.citationBritish Journal Of Pharmacology, 1992, v. 107 n. 2, p. 382-386en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171073-
dc.description.abstract1. The effects of the calmodulin antagonists, calmidazolium and fendiline were investigated on endothelium-dependent hyperpolarization in the canine coronary artery. The membrane potential of vascular smooth muscle cells was measured with the microelectrode technique. 2. Smooth muscle cells of the canine coronary artery had a resting membrane potential of -50 mV. Bradykinin and the Ca2+-ionophore, A23187, induced concentration- and endothelium-dependent hyperpolarization. The hyperpolarization induced by a supramaximal concentration of bradykinin (10-6 M) reached approximately 20 mV. 3. Calmidazolium (10-5 M) and fendiline (10-4 M) inhibited hyperpolarization induced by bradykinin and A23187. By contrast, calmidazolium did not affect the hyperpolarization induced by lemakalim, an opener of ATP-sensitive K+-channels. 4. These observations suggest that calmodulin is involved in the generation of endothelium-dependent membrane hyperpolarization of vascular smooth muscle.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBenzopyrans - Pharmacologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshCalmodulin - Antagonists & Inhibitorsen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshCromakalimen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFendiline - Pharmacologyen_US
dc.subject.meshImidazoles - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshPotassium Channels - Drug Effectsen_US
dc.subject.meshPyrroles - Pharmacologyen_US
dc.titleCalmodulin antagonists inhibit endothelium-dependent hyperpolarization in the canine coronary arteryen_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.doi10.1111/j.1476-5381.1992.tb12755.x-
dc.identifier.pmid1422587-
dc.identifier.scopuseid_2-s2.0-0026760157en_US
dc.identifier.volume107en_US
dc.identifier.issue2en_US
dc.identifier.spage382en_US
dc.identifier.epage386en_US
dc.identifier.isiWOS:A1992JQ85600019-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridNagao, T=7401489430en_US
dc.identifier.scopusauthoridIlliano, S=6602119848en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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