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Cardiovascular Research Advance Access [Accepted Manuscript] published online on November 24, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn322
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

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

Gui-Rong Li1,2, Hai-Ying Sun1, Xiao-Hua Zhang1, Lik-Cheung Cheng3, Shui-Wah Chiu3, Hung-Fat Tse1 and Chu-Pak Lau1

1 Department of Medicine and Research Centre of Heart, Brain, Hormone and Healthy Aging, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR China
2 Department of Physiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR China
3 Cardiothoracic Unit, Grantham Hospital, Li Ka Shing Faculty of Medicine, Pokfulam, The University of Hong Kong, Hong Kong SAR China

Correspondence to: Dr. Gui-Rong Li, Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR China, Tel: 852-2819-9513, Fax: 852-2855-9730; email: grli{at}hkucc.hku.hk

Aim: 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 IKur), and the voltage-gated sodium current (INa) in human atrial myocytes.

Methods: A whole-cell patch voltage clamp technique was employed to record Ito and IKur, and INa in human atrial myocytes.

Results: 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 (IC50: 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.

Conclusions: 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.

KEYWORDS Human; atrial myocytes; ion channels; omega-3 PUFAs

Time for primary review: 33 Days


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