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.

journal_name

Int J Cardiol

authors

Lin YK,Chen YC,Kao YH,Tsai CF,Yeh YH,Huang JL,Cheng CC,Chen SA,Chen YJ

doi

10.1016/j.ijcard.2014.07.004

subject

Has Abstract

pub_date

2014-09-01 00:00:00

pages

191-8

issue

1

eissn

0167-5273

issn

1874-1754

pii

S0167-5273(14)01194-2

journal_volume

176

pub_type

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