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钙通道拮抗剂对人神经母细胞瘤SH-SY5Y中[3H]去甲肾上腺素释放的影响。

The effect of calcium channel antagonists on the release of [3H]noradrenaline in the human neuroblastoma, SH-SY5Y.

作者信息

Murphy N P, Ball S G, Vaughan P F

机构信息

Department of Cardiovascular Studies, University of Leeds, U.K.

出版信息

Neurosci Lett. 1991 Aug 19;129(2):229-32. doi: 10.1016/0304-3940(91)90468-9.

Abstract

The effect of calcium channel antagonists on depolarization and carbachol evoked release of [3H]noradrenaline in the human neuroblastoma, SH-SY5Y, was investigated. Nifedipine, verapamil and diltiazem completely inhibited the depolarization evoked release of [3H]noradrenaline with IC50 values of 0.44 +/- 0.1 microM, 3.6 +/- 0.24 microM and 5.6 +/- 0.2 microM respectively. In addition, nickel, cobalt and cadmium, all at 2 mM, inhibited depolarization evoked release by 89.2 +/- 2.3%, 72.6 +/- 1.6% and 102.5 +/- 1.4% respectively. Furthermore, omega-conotoxin resulted in at least 20% inhibition of potassium evoked release, suggesting a role of N-type calcium channels. Carbachol evoked release of [3H]noradrenaline was inhibited by 10(-4) M nifedipine, diltiazem and verapamil by 15.6 +/- 1.1%, 14.6 +/- 3.2% and 23.6 +/- 1.8% respectively and by 2 mM nickel, cobalt and cadmium by 13.8 +/- 3.2%, 34 +/- 2.1% and 6.5 +/- 3.7% respectively. These results suggest that depolarization evoked release of [3H]noradrenaline is mediated via L- and N-type calcium channels, whereas, carbachol evoked release does not appear to be coupled an L-, T- or N-type voltage sensitive calcium channel.

摘要

研究了钙通道拮抗剂对人神经母细胞瘤SH - SY5Y细胞去极化及卡巴胆碱诱发的[3H]去甲肾上腺素释放的影响。硝苯地平、维拉帕米和地尔硫卓完全抑制去极化诱发的[3H]去甲肾上腺素释放,IC50值分别为0.44±0.1微摩尔/升、3.6±0.24微摩尔/升和5.6±0.2微摩尔/升。此外,镍、钴和镉在2毫摩尔浓度时,分别使去极化诱发的释放抑制89.2±2.3%、72.6±1.6%和102.5±1.4%。此外,ω -芋螺毒素至少使钾离子诱发的释放抑制20%,提示N型钙通道起作用。卡巴胆碱诱发的[3H]去甲肾上腺素释放,10−4摩尔/升的硝苯地平、地尔硫卓和维拉帕米分别抑制15.6±1.1%、14.6±3.2%和23.6±1.8%,2毫摩尔的镍、钴和镉分别抑制13.8±3.2%、34±2.1%和6.5±3.7%。这些结果表明,去极化诱发的[3H]去甲肾上腺素释放是通过L型和N型钙通道介导的,而卡巴胆碱诱发的释放似乎与L型、T型或N型电压敏感性钙通道无关。

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