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Article: Effects of U50,488H on transient outward and ultra-rapid delayed rectifier K+ currents in young human atrial myocytes

TitleEffects of U50,488H on transient outward and ultra-rapid delayed rectifier K+ currents in young human atrial myocytes
Authors
KeywordsAtrium, human
Ion channel
K+ current, transient outward
K+ current, ultra-rapid delayed rectifier
Opioid
U50,488H
Issue Date2003
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2003, v. 473 n. 2-3, p. 97-103 How to Cite?
AbstractThe effects of trans-(±)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]- benzeneacetamide methanesulfonate salt (U50,488H), a selective κ-opioid receptor agonist, on transient outward K+ current (Ito1) and ultra-rapid delayed rectifier K+ current (IKur) in young human atrial myocytes were evaluated with a whole-cell patch-clamp technique. At +10 mV, U50,488H decreased Ito1 in a concentration-dependent manner (IC50=12.4±3.5 μM), while at +50 mV, U50,488H produced biphasic effects on Ito1 - increasing and decreasing the current at 1-3 and 10-30 μM, respectively. U50,488H at 10 μM shifted the midpoint (V0.5) of Ito1 activation in a depolarizing direction by ∼5 mV, accelerated the inactivation, and slowed the recovery from inactivation of Ito1. In addition, U50,488H inhibited IKur in a concentration-dependent manner (IC50=3.3±0.6 μM). The effects of U50,488H on the two types of K+ currents were not antagonized by either 5 μM nor-binaltorphimine or 300 nM naloxone. These results indicate that U50,488H affects both Ito1 and IKur in young human atrial myocytes in an opioid receptor-independent manner. © 2003 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/85489
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXiao, GSen_HK
dc.contributor.authorZhou, JJen_HK
dc.contributor.authorCheung, YFen_HK
dc.contributor.authorLi, GRen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2010-09-06T09:05:41Z-
dc.date.available2010-09-06T09:05:41Z-
dc.date.issued2003en_HK
dc.identifier.citationEuropean Journal Of Pharmacology, 2003, v. 473 n. 2-3, p. 97-103en_HK
dc.identifier.issn0014-2999en_HK
dc.identifier.urihttp://hdl.handle.net/10722/85489-
dc.description.abstractThe effects of trans-(±)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]- benzeneacetamide methanesulfonate salt (U50,488H), a selective κ-opioid receptor agonist, on transient outward K+ current (Ito1) and ultra-rapid delayed rectifier K+ current (IKur) in young human atrial myocytes were evaluated with a whole-cell patch-clamp technique. At +10 mV, U50,488H decreased Ito1 in a concentration-dependent manner (IC50=12.4±3.5 μM), while at +50 mV, U50,488H produced biphasic effects on Ito1 - increasing and decreasing the current at 1-3 and 10-30 μM, respectively. U50,488H at 10 μM shifted the midpoint (V0.5) of Ito1 activation in a depolarizing direction by ∼5 mV, accelerated the inactivation, and slowed the recovery from inactivation of Ito1. In addition, U50,488H inhibited IKur in a concentration-dependent manner (IC50=3.3±0.6 μM). The effects of U50,488H on the two types of K+ currents were not antagonized by either 5 μM nor-binaltorphimine or 300 nM naloxone. These results indicate that U50,488H affects both Ito1 and IKur in young human atrial myocytes in an opioid receptor-independent manner. © 2003 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_HK
dc.relation.ispartofEuropean Journal of Pharmacologyen_HK
dc.rightsEuropean Journal of Pharmacology. Copyright © Elsevier BV.en_HK
dc.subjectAtrium, humanen_HK
dc.subjectIon channelen_HK
dc.subjectK+ current, transient outwarden_HK
dc.subjectK+ current, ultra-rapid delayed rectifieren_HK
dc.subjectOpioiden_HK
dc.subjectU50,488Hen_HK
dc.subject.mesh3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer - pharmacologyen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshChilden_HK
dc.subject.meshChild, Preschoolen_HK
dc.subject.meshDelayed Rectifier Potassium Channelsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHeart Atriaen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInfanten_HK
dc.subject.meshMaleen_HK
dc.subject.meshMyocytes, Cardiac - drug effects - physiologyen_HK
dc.subject.meshNaloxone - pharmacologyen_HK
dc.subject.meshNaltrexone - analogs & derivatives - pharmacologyen_HK
dc.subject.meshNarcotic Antagonists - pharmacologyen_HK
dc.subject.meshPatch-Clamp Techniquesen_HK
dc.subject.meshPotassium Channels - drug effects - physiologyen_HK
dc.subject.meshPotassium Channels, Tandem Pore Domainen_HK
dc.subject.meshPotassium Channels, Voltage-Gateden_HK
dc.subject.meshReceptors, Opioid, kappa - agonistsen_HK
dc.titleEffects of U50,488H on transient outward and ultra-rapid delayed rectifier K+ currents in young human atrial myocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-2999&volume=473&issue=2-3&spage=97&epage=103&date=2003&atitle=Effects+of+U50,488H+on+transient+outward+and+ultra-rapid+delayed+rectifier+K++currents+in+young+human+atrial+myocytesen_HK
dc.identifier.emailCheung, YF:xfcheung@hku.hken_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityCheung, YF=rp00382en_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0014-2999(03)01974-5en_HK
dc.identifier.pmid12892826-
dc.identifier.scopuseid_2-s2.0-0042206733en_HK
dc.identifier.hkuros84046en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0042206733&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume473en_HK
dc.identifier.issue2-3en_HK
dc.identifier.spage97en_HK
dc.identifier.epage103en_HK
dc.identifier.isiWOS:000184564900002-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridXiao, GS=8695315100en_HK
dc.identifier.scopusauthoridZhou, JJ=7405545441en_HK
dc.identifier.scopusauthoridCheung, YF=7202111067en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.scopusauthoridWong, TM=7403531434en_HK

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