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.
journal_name
Int J Cardioljournal_title
International journal of cardiologyauthors
Lin YK,Chen YC,Kao YH,Tsai CF,Yeh YH,Huang JL,Cheng CC,Chen SA,Chen YJdoi
10.1016/j.ijcard.2014.07.004subject
Has Abstractpub_date
2014-09-01 00:00:00pages
191-8issue
1eissn
0167-5273issn
1874-1754pii
S0167-5273(14)01194-2journal_volume
176pub_type
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