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Article: Omega-3 polyunsaturated fatty acids inhibit transient outward and ultra-rapid delayed rectifier K+ currents and Na+ current in human atrial myocytes

TitleOmega-3 polyunsaturated fatty acids inhibit transient outward and ultra-rapid delayed rectifier K+ currents and Na+ current in human atrial myocytes
Authors
Li, GRSun, HYZhang, XHCheng, LCChiu, SWTse, HFLau, CP
KeywordsAtrial myocytes
Human
Ion channels
Omega-3 PUFAs
Issue Date2009
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 2009, v. 81 n. 2, p. 286-293 How to Cite?
DOI: http://dx.doi.org/10.1093/cvr/cvn322
AbstractAims: The omega-3 (n-3) polyunsaturated fatty acids (omega-3 PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from fish oil were recently reported to have an anti-atrial fibrillation effect in humans; however, the ionic mechanisms of this effect are not fully understood. The present study was designed to determine the effects of EPA and DHA on transient outward and ultra-rapid delayed rectifier potassium currents (Ito and I Kur) and the voltage-gated sodium current (INa) in human atrial myocytes. Methods and results: A whole-cell patch voltage clamp technique was employed to record Ito and IKur, and INa in human atrial myocytes. It was found that EPA and DHA inhibited Ito in a concentration-dependent manner (IC50: 6.2 μM for EPA; 4.1 μM for DHA) and positively shifted voltage-dependent activation of the current. In addition, IKur was suppressed by 1-50 μM EPA (IC 50: 17.5 μM) and DHA (IC50: 4.3 μM). Moreover, EPA and DHA reduced INa in human atrial myocytes in a concentration-dependent manner (IC50: 10.8 μM for EPA; 41.2 μM for DHA) and negatively shifted the potential of INa availability. The INa block by EPA or DHA was use-independent. Conclusion: The present study demonstrates for the first time that EPA and DHA inhibit human atrial Ito, IKur, and INa in a concentration-dependent manner; these effects may contribute, at least in part, to the anti-atrial fibrillation of omega-3 PUFAs in humans. © The Author 2008.
Persistent Identifierhttp://hdl.handle.net/10722/59170
ISSN
0008-6363
2023 Impact Factor: 10.2
2023 SCImago Journal Rankings: 2.809
ISI Accession Number ID
WOS:000262518600010
Funding AgencyGrant Number
Sun Chieh Yeh Heart Foundation of Hong Kong
Funding Information:

The work was supported by Sun Chieh Yeh Heart Foundation of Hong Kong.

References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_HK
dc.contributor.authorSun, HYen_HK
dc.contributor.authorZhang, XHen_HK
dc.contributor.authorCheng, LCen_HK
dc.contributor.authorChiu, SWen_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorLau, CPen_HK
dc.date.accessioned2010-05-31T03:44:14Z-
dc.date.available2010-05-31T03:44:14Z-
dc.date.issued2009en_HK
dc.identifier.citationCardiovascular Research, 2009, v. 81 n. 2, p. 286-293en_HK
dc.identifier.issn0008-6363en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59170-
dc.description.abstractAims: The omega-3 (n-3) polyunsaturated fatty acids (omega-3 PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from fish oil were recently reported to have an anti-atrial fibrillation effect in humans; however, the ionic mechanisms of this effect are not fully understood. The present study was designed to determine the effects of EPA and DHA on transient outward and ultra-rapid delayed rectifier potassium currents (Ito and I Kur) and the voltage-gated sodium current (INa) in human atrial myocytes. Methods and results: A whole-cell patch voltage clamp technique was employed to record Ito and IKur, and INa in human atrial myocytes. It was found that EPA and DHA inhibited Ito in a concentration-dependent manner (IC50: 6.2 μM for EPA; 4.1 μM for DHA) and positively shifted voltage-dependent activation of the current. In addition, IKur was suppressed by 1-50 μM EPA (IC 50: 17.5 μM) and DHA (IC50: 4.3 μM). Moreover, EPA and DHA reduced INa in human atrial myocytes in a concentration-dependent manner (IC50: 10.8 μM for EPA; 41.2 μM for DHA) and negatively shifted the potential of INa availability. The INa block by EPA or DHA was use-independent. Conclusion: The present study demonstrates for the first time that EPA and DHA inhibit human atrial Ito, IKur, and INa in a concentration-dependent manner; these effects may contribute, at least in part, to the anti-atrial fibrillation of omega-3 PUFAs in humans. © The Author 2008.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_HK
dc.relation.ispartofCardiovascular Researchen_HK
dc.rightsCardiovascular Research. Copyright © Elsevier BV.en_HK
dc.subjectAtrial myocytes-
dc.subjectHuman-
dc.subjectIon channels-
dc.subjectOmega-3 PUFAs-
dc.subject.meshDelayed Rectifier Potassium Channels - antagonists & inhibitorsen_HK
dc.subject.meshDocosahexaenoic Acids - pharmacologyen_HK
dc.subject.meshEicosapentaenoic Acid - pharmacologyen_HK
dc.subject.meshHeart Atria - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMyocytes, Cardiac - drug effects - metabolismen_HK
dc.subject.meshPotassium Channel Blockers - pharmacologyen_HK
dc.subject.meshSodium Channel Blockers - pharmacologyen_HK
dc.titleOmega-3 polyunsaturated fatty acids inhibit transient outward and ultra-rapid delayed rectifier K+ currents and Na+ current in human atrial myocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-6363&volume=81&issue=2&spage=286&epage=93&date=2009&atitle=Omega-3+polyunsaturated+fatty+acids+inhibit+transient+outward+and+ultra-rapid+delayed+rectifier+K++currents+and+Na++current+in+human+atrial+myocytes.en_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/cvr/cvn322en_HK
dc.identifier.pmid19029136en_HK
dc.identifier.scopuseid_2-s2.0-58449121898en_HK
dc.identifier.hkuros156314en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58449121898&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume81en_HK
dc.identifier.issue2en_HK
dc.identifier.spage286en_HK
dc.identifier.epage293en_HK
dc.identifier.eissn1755-3245-
dc.identifier.isiWOS:000262518600010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.f1000717297966-
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.scopusauthoridSun, HY=35723049200en_HK
dc.identifier.scopusauthoridZhang, XH=7410270356en_HK
dc.identifier.scopusauthoridCheng, LC=9533935800en_HK
dc.identifier.scopusauthoridChiu, SW=12788356600en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.issnl0008-6363-

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