Differential effects of Ca2+ channel blockers on Ca2+ overload induced by lysophosphatidylcholine in cardiomyocytes
Differential effects of Ca2+ channel blockers on Ca2+ overload induced by lysophosphatidylcholine in cardiomyocytes
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DOI：
10.1016/s0014-2999(97)01138-2
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发表时间：
1997-08-27
影响因子：
5
通讯作者：
Abiko, Y
中科院分区：
文献类型：
--
作者：
Chen, M;Xiao, CY;Abiko, Y
The effects of Ca2+ channel blockers (verapamil, diltiazem, nicardipine, bepridil and flunarizine) on Ca2+ overload induced by lysophosphatidylcholine were examined in rat isolated cardiomyocytes. Addition of lysophosphatidylcholine (15 mu M) produced Ca2+ overload as evidenced by a marked increase in the concentration of intracellular Ca2+ and hypercontracture of cells. Verapamil, flunarizine and bepridil concentration dependently inhibited the lysophosphatidylcholine-induced Ca2+ overload, whereas diltiazem and nicardipine did not. Lysophosphatidylcholine increased the release of creatine kinase, which was significantly attenuated by verapamil, flunarizine or bepridil (5 mu M for each), but not by diltiazem or nicardipine (20 mu M for each). Verapamil, flunarizine, bepridil (which attenuated the lysophosphatidylcholine-induced Ca2+ overload) and nicardipine (which did not) inhibited the veratridine-induced increase in the concentration of intracellular Na+ (indicated by the increase in fluorescence ratio of Na+-binding benzofuran isophthalate) and cell contracture, whereas diltiazem did not. These results suggest that verapamil, bepridil and flunarizine attenuate the Ca2+ overload induced by lysophosphatidylcholine, and that the Ca2+ channel blocking action of these drugs does not contribute substantially to this effect. The Na+ channel inhibition together with high lipophilicity of these drugs may be important for the attenuation of the lysophosphatidylcholine-induced Ca2+ overload. (C) 1997 Elsevier Science B.V.
