title: A monounsaturated fatty acid (oleic acid) modulates electrical activity in atrial myocytes with calcium and sodium dysregulation.
abstract: BACKGROUND
  Obesity and metabolic syndrome are important risk factors for atrial fibrillation. High plasma concentrations of monounsaturated fatty acids, including oleic acid (OLA), are frequently noted in obese individuals and patients with metabolic syndrome. However, it is not clear whether monounsaturated fatty acids (MUFAs) can directly modulate the electrophysiological characteristics of atrial myocytes.
  
  
  METHODS
  Whole-cell patch clamp, indo-1 fluorescence, and Western blot analyses were used to record the action potentials (APs), ionic currents, and protein expressions of HL-1 myocytes incubated with and without (control) OLA (0.5mM) for 24h.
  
  
  RESULTS
  Compared to control myocytes (n=14), OLA-treated myocytes (n=16) had shorter APD90 (65 ± 6 vs. 85 ± 6 ms, p<0.05) and APD50 (24 ± 6 vs. 38 ± 4 ms, p<0.05) with a higher incidence of delayed afterdepolarizations (35.7% vs. 7%, p<0.05), which were suppressed by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, a blocker of the calcium-activated chloride current). In addition, OLA-treated myocytes (n=19) exhibited larger calcium transients (0.54 ± 0.06 vs. 0.38 ± 0.05 R410/485, p<0.05), and sarcoplasmic reticular calcium contents (0.91 ± 0.05 vs. 0.64 ± 0.08 R410/485, p<0.05) than control myocytes (n=15). OLA-treated myocytes had larger late sodium currents, smaller sodium-calcium exchanger currents, and smaller sodium-potassium pump currents. Moreover OLA-treated myocytes had higher expressions of sarcoplasmic reticular Ca(2+)-ATPase and calmodulin kinase II, but lower expression of the sodium-potassium ATPase protein than control myocytes.
  
  
  CONCLUSIONS
  MUFAs can regulate atrial electrophysiological characteristics with calcium and sodium dysregulation, which may contribute to atrial arrhythmogenesis.
authors: Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
authors: Yung-Kuo
authors: YK
authors: Lin
authors: Department of Biomedical Engineering, National Defense Medical Center, Taipei, Taiwan.
authors: Yao-Chang
authors: YC
authors: Chen
authors: Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Medical Education and Research, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
authors: Yu-Hsun
authors: YH
authors: Kao
authors: Division of Cardiology, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan; School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
authors: Chin-Feng
authors: CF
authors: Tsai
authors: The First Cardiovascular Division, Chang-Gung Memorial Hospital, Chang-Gung University, Taoyuan, Taiwan.
authors: Yung-Hsin
authors: YH
authors: Yeh
authors: Cardiovascular Center, Taichung Veterans General Hospital, Taichung, Taiwan; Faculty of Medicine and Institute of Clinical Medicine, and Cardiovascular Research Institute, National Yang-Ming University, Taipei, Taiwan.
authors: Jin-Long
authors: JL
authors: Huang
authors: Division of Cardiology, Chi-Mei Hospital, Tainan, Taiwan.
authors: Chen-Chuan
authors: CC
authors: Cheng
authors: National Yang-Ming University, School of Medicine, Division of Cardiology and Cardiovascular Research Center, Veterans General Hospital-Taipei, Taipei, Taiwan.
authors: Shih-Ann
authors: SA
authors: Chen
authors: Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. Electronic address: yjchen@tmu.edu.tw.
authors: Yi-Jen
authors: YJ
authors: Chen
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology*; D002478:Cells, Cultured; D051379:Mice; D032383:Myocytes, Cardiac / Q000187:drug effects*; D019301:Oleic Acid / Q000494:pharmacology* / Q000633:toxicity; D012964:Sodium / Q000502:physiology*; D019831:Sodium-Calcium Exchanger / Q000502:physiology*
chemical_list: D019831:Sodium-Calcium Exchanger; D019301:Oleic Acid; D012964:Sodium; D002118:Calcium
keywords: Atrial fibrillation; Obesity; Oleic acid