Li S N, Bräter M, Andreas K
Institute of Pharmacology and Toxicology, Dresden University of Technology, Germany.
Neurosci Lett. 1997 Jul 18;230(2):85-8. doi: 10.1016/s0304-3940(97)00481-3.
The effects of nifedipine, niguldipine, nimodipine and nitrendipine on the high K+-induced intracellular Ca2+ ([Ca2+]i) transient in dibutyryl cAMP-differentiated neuroblastoma x glioma hybrid NG 108-15 cells were studied by using the fluorescent Ca2+ indicator fura-2. It was observed that nifedipine at the concentration of 50 microM inhibited the high K+-induced [Ca2+]i transient by about 60%; niguldipine at the concentration of 10 microM caused a reduction of about 65% in the high K+-induced calcium signal and a further increase in the concentration up to 50 microM did not result in a significant further reduction in the high K+-induced calcium signal. However, on the other hand, nimodipine and nitrendipine at 50 microM inhibited almost completely the high K+-induced [Ca2+]i transient. Consequently, it was demonstrated in the present study that nimodipine and nitrendipine inhibit both L- and N-type calcium channels and thus seem to be unique among the dihydropyridines examined in their effects on calcium channels in dibutyryl cAMP-differentiated neuroblastoma x glioma hybrid NG 108-15 cells, whereas nifedipine and niguldipine appear to block mainly L-type calcium channels.
利用荧光钙指示剂fura-2研究了硝苯地平、尼鲁地平、尼莫地平和尼群地平对二丁酰环磷腺苷分化的神经母细胞瘤x胶质瘤杂交细胞NG 108-15中高钾诱导的细胞内钙（[Ca2+]i）瞬变的影响。观察到，浓度为50微摩尔的硝苯地平可使高钾诱导的[Ca2+]i瞬变抑制约60%；浓度为10微摩尔的尼鲁地平可使高钾诱导的钙信号降低约65%，浓度进一步增加至50微摩尔时，高钾诱导的钙信号并未显著进一步降低。然而，另一方面，50微摩尔的尼莫地平和尼群地平几乎完全抑制了高钾诱导的[Ca2+]i瞬变。因此，本研究表明，尼莫地平和尼群地平抑制L型和N型钙通道，因此在所研究的二氢吡啶类药物中，它们对二丁酰环磷腺苷分化的神经母细胞瘤x胶质瘤杂交细胞NG 108-15中钙通道的作用似乎是独特的，而硝苯地平和尼鲁地平似乎主要阻断L型钙通道。
