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首页> 外文期刊>Research communications in molecular pathology and pharmacology >Facilitation of calcium influx by propylene glycol through the voltage-dependent calcium channels in PC12 cells.
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Facilitation of calcium influx by propylene glycol through the voltage-dependent calcium channels in PC12 cells.

机译:通过PC12细胞中电压依赖性钙通道,丙二醇促进钙内流。

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摘要

Propylene glycol (PG) raises an intracellular calcium concentration ([Ca2+]i) in PC12 cells. The present study has been undertaken to examine whether or not the voltage-dependent Ca2+ channels are involved in the PG-induced rise in [Ca2+]i and, if so, to determine which types participate in it. CdCl2 (50 micro M) and the Ca2+ -free saline depressed the action of PG (0.5 - 10 %v/v)-induced [Ca2+]i rise. Although NiCl2 (50 micro M) at the same concentration as CdCl2, and omega-agatoxin (50 and 300 nM) had no effect on the PG-induced [Ca2+]i rise, each of omega-conotoxin (1 micro M), nifedipine (10 micro M), nicardipine (10 micro M), varapamil (10 micro M) and diltiazem (10 micro M) significantly decreased it. Electrical stimulation and Bay K 8644 (1 micro M) enhanced the PG-induced [Ca2+]i rise. The second phase of the [Ca2]i rise was fallen fast by nicardipine (10 micro M), but not by omega-conotoxin (1 micro M). The results obtained suggested that the Ca2+ influx through the L- and N-type Ca2+ channels are involved in the PG-induced [Ca2+]i rise.
机译:丙二醇(PG)提高PC12细胞中的细胞内钙浓度([Ca2 +] i)。本研究已进行以检查电压依赖性Ca2 +通道是否参与PG诱导的[Ca2 +] i升高,如果是,则确定哪些类型参与其中。 CdCl2(50 micro M)和不含Ca2 +的盐水抑制了PG(0.5-10%v / v)诱导的[Ca2 +] i升高的作用。尽管浓度与CdCl2相同的NiCl2(50 micro M)和ω-agatoxin(50和300 nM)对PG诱导的[Ca2 +] i升高没有影响,但每个omega-conotoxin(1 micro M),硝苯地平(10微米),尼卡地平(10微米),瓦拉帕米(10微米)和地尔硫卓(10微米)显着降低了它。电刺激和Bay K 8644(1 micro M)增强了PG诱导的[Ca2 +] i升高。尼卡地平(10 micro M)使[Ca2] i上升的第二阶段快速下降,但ω-芋螺毒素(1 micro M)没有迅速下降。获得的结果表明,通过L型和N型Ca2 +通道的Ca2 +流入与PG诱导的[Ca2 +] i升高有关。

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