高渗性钙通过电压依赖性钙通道内流

Hattori Toshimi
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引用次数: 1

摘要

我们发现丙二醇(PG)提高细胞内钙浓度([Ca2+]i), PG诱导的高渗性参与了[Ca2+]i的升高。本研究旨在确定通过Ca2+通道的Ca2+内流是否与高渗性引起的[Ca2+]i升高有关。无Ca2+生理盐水和所有Ca2+通道阻滞剂CdCl2 (0.1 mM), o- concontoxin GVIA(1µM),维拉帕米(10µM)和尼卡地平(10µM)显著降低高张力引起的[Ca2+]i。Bay K 8644(4µM),一种Ca2+通道激活剂,可能增加高渗盐引起的[Ca2+]i。上述结果使我得出结论,通过电压依赖性Ca2+通道的Ca2+内流参与了高张力诱导的[Ca2+]i升高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Calcium influx by hypertonicity through the voltage-dependent calcium channels
We found out before the facts that propylene glycol (PG) raises the intracellular calcium concentration ([Ca2+]i) and that hypertonicity induced by PG is involved in the [Ca2+]i rise. The present study was conducted for the purpose of determining whether the Ca2+ influx through the Ca2+ channels is related to the rise in [Ca2+]i incuded by hypertonicity. A Ca2+-free saline and all of the Ca2+ channel blockers CdCl2 (0.1 mM), o-conotoxin GVIA (1 µM), verapamil (10 µM), and nicardipine (10 µM) significantly decreased the [Ca2+]i raised by hypertonicity. Bay K 8644 (4 µM), a Ca2+ channel activator, potentially increased the [Ca2+]i raised by hypertonic salines. The results described above lead me to the conclusion that the Ca2+ influx through the voltage-dependent Ca2+ channels is involved in the hypertonicity-induced [Ca2+]i rise.
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