Effects of oleic acid on the high threshold barium current in seabass Dicentrarchus labrax ventricular myocytes
| Type | Article | ||||||||
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| Date | 2006-10 | ||||||||
| Language | English | ||||||||
| Author(s) | Chatelier Aurelien1, Imbert Nathalie1, Zambonino-Infante Jose-Luis 2, McKenzie David3, Bois P4 |
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| Affiliation(s) | 1 : Univ La Rochelle, Lab Biol & Environm Marin, F-17042 La Rochelle, France. 2 : IFREMER, INRA, Unite Mixre Nutr Poissons, F-29280 Plouzane, France. 3 : Danish Inst fisheries Res, N Seas Ctr, Dept Marine Ecol & Aquaculture, DK-9850 Hirtshals, Denmark. 4 : Univ Poitiers, UMR 6187, CNRS, Inst Physiol & Biol Cellulaire, F-86022 Poitiers, France. |
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| Source | Journal of Experimental Biology (0022-0949) (The Company of Biologists), 2006-10 , Vol. 209 , N. 20 , P. 4033-4039 | ||||||||
| DOI | 10.1242/jeb.02470 | ||||||||
| WOS© Times Cited | 7 | ||||||||
| Keyword(s) | Fatty acid, Sea bass, Ventricular myocyte, L type calcium channel, Oleic acid | ||||||||
| Abstract | The present study employed a patch clamp technique in isolated seabass ventricular myocytes to investigate the hypothesis that oleic acid (OA), a mono-unsaturated fatty acid, can exert direct effects upon whole-cell barium currents. Acute application of free OA caused a dose-dependent depression of the whole-cell barium current that was evoked by a voltage step to 0 mV from a holding potential of -80 mV. The derived 50% inhibitory concentration (IC50) was 12.49 +/- 0.27 mu mol l(-1). At a concentration of 30 mu mol l(-1), OA significantly reduced the current density to about 45% of control values, but did not modify either the shape of the current-density voltage relationship or the apparent reversal potential. In addition, OA did not modify the voltage dependence of either steady state inactivation or activation curves. Taken together, these results indicate that physiological concentrations of free OA decrease the conductance of the L-type inward current, without altering its properties of selectivity and its voltage dependence. The inhibitory effect of OA upon the L-type calcium channel may translate, in vivo, into a protective effect against arrhythmias induced by Ca2+ overload. | ||||||||
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