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Article: Pharmacology of Cardiac Potassium Channels

TitlePharmacology of Cardiac Potassium Channels
Authors
Keywords4-AP
AF
Antiarrhythmic drugs
APD
CaMKII
Cardiac arrhythmias
Cardiomyocytes
EADs
ECG
EGFR
ERP
HERG
IKACh
IKATP
IKr
IKs
IKur
Ito1
K2p
K+ channels
Kir
LQTs
MitoKATP
Pharmacology
PIP2
PKA
PKC
PLC
PTK
SarcKATP
SQTs
SUR
TdPs
TMD
Issue Date2010
PublisherAcademic Press.
Citation
Advances In Pharmacology, 2010, v. 59 C, p. 93-134 How to Cite?
AbstractCardiac K+ channels are cardiomyocyte membrane proteins that regulate K+ ion flow across the cell membrane on the electrochemical gradient and determine the resting membrane potential and the cardiac action potential morphology and duration. Several K+ channels have been well studied in the human heart. They include the transient outward K+ current Ito1, the ultra-rapidly activating delayed rectifier current IKur, the rapidly and slowly activating delayed rectifier currents IKr and IKs, the inward rectifier K+ current IK1, and ligand-gated K+ channels, including adenosine-5'-triphosphate (ATP)-sensitive K+ current (IKATP) and acetylcholine-activated current (IKACh). Regional differences of K+ channel expression contribute to the variable morphologies and durations of cardiac action potentials from sinus node and atrial to ventricular myocytes, and different ventricular layers from endocardium and midmyocardium to epicardium. They also show different responses to endogenous regulators and/or pharmacological agents. K+ channels are well-known targets for developing novel anti-arrhythmic drugs that can effectively prevent/inhibit cardiac arrhythmias. Especially, atrial-specific K+ channel currents (IKur and IKACh) are the targets for developing atrial-selective anti-atrial fibrillation drugs, which has been greatly progressed in recent years. This chapter concentrates on recent advances in intracellular signaling regulation and pharmacology of cardiac K+ channels under physiological and pathophysiological conditions. © 2010 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/130436
ISSN
2015 SCImago Journal Rankings: 1.718
References

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_HK
dc.contributor.authorDong, MQen_HK
dc.date.accessioned2010-12-23T08:52:04Z-
dc.date.available2010-12-23T08:52:04Z-
dc.date.issued2010en_HK
dc.identifier.citationAdvances In Pharmacology, 2010, v. 59 C, p. 93-134en_HK
dc.identifier.issn1054-3589en_HK
dc.identifier.urihttp://hdl.handle.net/10722/130436-
dc.description.abstractCardiac K+ channels are cardiomyocyte membrane proteins that regulate K+ ion flow across the cell membrane on the electrochemical gradient and determine the resting membrane potential and the cardiac action potential morphology and duration. Several K+ channels have been well studied in the human heart. They include the transient outward K+ current Ito1, the ultra-rapidly activating delayed rectifier current IKur, the rapidly and slowly activating delayed rectifier currents IKr and IKs, the inward rectifier K+ current IK1, and ligand-gated K+ channels, including adenosine-5'-triphosphate (ATP)-sensitive K+ current (IKATP) and acetylcholine-activated current (IKACh). Regional differences of K+ channel expression contribute to the variable morphologies and durations of cardiac action potentials from sinus node and atrial to ventricular myocytes, and different ventricular layers from endocardium and midmyocardium to epicardium. They also show different responses to endogenous regulators and/or pharmacological agents. K+ channels are well-known targets for developing novel anti-arrhythmic drugs that can effectively prevent/inhibit cardiac arrhythmias. Especially, atrial-specific K+ channel currents (IKur and IKACh) are the targets for developing atrial-selective anti-atrial fibrillation drugs, which has been greatly progressed in recent years. This chapter concentrates on recent advances in intracellular signaling regulation and pharmacology of cardiac K+ channels under physiological and pathophysiological conditions. © 2010 Elsevier Inc.en_HK
dc.languageengen_US
dc.publisherAcademic Press.-
dc.relation.ispartofAdvances in Pharmacologyen_HK
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in Advances in Pharmacology . Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Advances in Pharmacology , 2010, v. 59, p. 93-134. DOI: 10.1016/S1054-3589(10)59004-5-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject4-APen_HK
dc.subjectAFen_HK
dc.subjectAntiarrhythmic drugsen_HK
dc.subjectAPDen_HK
dc.subjectCaMKIIen_HK
dc.subjectCardiac arrhythmiasen_HK
dc.subjectCardiomyocytesen_HK
dc.subjectEADsen_HK
dc.subjectECGen_HK
dc.subjectEGFRen_HK
dc.subjectERPen_HK
dc.subjectHERGen_HK
dc.subjectIKAChen_HK
dc.subjectIKATPen_HK
dc.subjectIKren_HK
dc.subjectIKsen_HK
dc.subjectIKuren_HK
dc.subjectIto1en_HK
dc.subjectK2pen_HK
dc.subjectK+ channelsen_HK
dc.subjectKiren_HK
dc.subjectLQTsen_HK
dc.subjectMitoKATPen_HK
dc.subjectPharmacologyen_HK
dc.subjectPIP2en_HK
dc.subjectPKAen_HK
dc.subjectPKCen_HK
dc.subjectPLCen_HK
dc.subjectPTKen_HK
dc.subjectSarcKATPen_HK
dc.subjectSQTsen_HK
dc.subjectSURen_HK
dc.subjectTdPsen_HK
dc.subjectTMDen_HK
dc.subject.meshAction Potentials - drug effects - physiology-
dc.subject.meshAnti-Arrhythmia Agents - chemistry - pharmacology - therapeutic use-
dc.subject.meshArrhythmias, Cardiac - drug therapy - metabolism - physiopathology-
dc.subject.meshIon Channel Gating - drug effects - physiology-
dc.subject.meshPotassium Channels - drug effects - physiology-
dc.titlePharmacology of Cardiac Potassium Channelsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1054-3589&volume=59&spage=93&epage=134&date=2010&atitle=Pharmacology+of+cardiac+potassium+channels-
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1016/S1054-3589(10)59004-5en_HK
dc.identifier.pmid20933200-
dc.identifier.scopuseid_2-s2.0-77957365025en_HK
dc.identifier.hkuros183257en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77957365025&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume59en_HK
dc.identifier.issueCen_HK
dc.identifier.spage93en_HK
dc.identifier.epage134en_HK
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.scopusauthoridDong, MQ=7202127303en_HK

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