caa a22 4500 469079509 CHVBK 20180323132945.0 cr unu---uuuuu 170328e19920401xx s 000 0 eng 10.1007/BF00176628 doi (NATIONALLICENCE)springer-10.1007/BF00176628 Modification by solvents of the action of nifedipine on calcium channel currents in neuroblastoma cells [Elektronische Daten] [Lingyun Wu, Edward Karpinski, Rui Wang, Peter Pang] Summary: The effect of nifedipine dissolved in different solvents on the two types of calcium channel currents in neuroblastoma cells was investigated using the whole cell version of the patch clamp technique. Nifedipine dissolved in dimethylsulfoxide (nifedipine/DMSO) decreased the transient calcium channel (T channel) current by 50% at a concentration of 10 μM. This inhibitory effect was concentration-dependent and reversible. In contrast, T channel currents were not inhibited by nifedipine at a similar concentration dissolved in acetone or ethanol. Further experiments were carried out with dried nifedipine/DMSO. Dried nifedipine/DMSO powder re-dissolved in acetone or ethanol at a concentration of 10 μM decreased the T channel current by 32% and 37%, respectively. In addition, within the concentration range of 10 nM to 100 μM nifedipine/DMSO inhibited the long-lasting calcium channel (L channel) current more effectively than did nifedipine dissolved in acetone. The concentration of solvent (DMSO, ethanol, acetone) in the bath was fixed at 0.3% to reach different final concentrations of nifedipine. Solvents alone at a final concentration of 0.3% did not show any effect on T or L channel currents. UV absorbance measurements indicated that the combination of nifedipine, solvent and bath solution did not result in precipitation of the dihydropyridine during the experimental protocol. It is concluded that when DMSO is used as the solvent, nifedipine is not only a more effective L channel antagonist but also a T channel antagonist in neuroblastoma cells. Springer-Verlag, 1992 Nifedipine nationallicence T Channel currents nationallicence Solvents nationallicence Neuroblastoma cell nationallicence Wu Lingyun Department of Physiology, University of Alberta, T6G 2H7, Edmonton, Alberta, Canada aut Karpinski Edward Department of Physiology, University of Alberta, T6G 2H7, Edmonton, Alberta, Canada aut Wang Rui Department of Physiology, University of Alberta, T6G 2H7, Edmonton, Alberta, Canada aut Pang Peter Department of Physiology, University of Alberta, T6G 2H7, Edmonton, Alberta, Canada aut Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 345/4(1992-04-01), 478-484 0028-1298 345:4<478 1992 345 210 https://doi.org/10.1007/BF00176628 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00176628 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Wu Lingyun Department of Physiology, University of Alberta, T6G 2H7, Edmonton, Alberta, Canada aut NATIONALLICENCE 700 1- Karpinski Edward Department of Physiology, University of Alberta, T6G 2H7, Edmonton, Alberta, Canada aut NATIONALLICENCE 700 1- Wang Rui Department of Physiology, University of Alberta, T6G 2H7, Edmonton, Alberta, Canada aut NATIONALLICENCE 700 1- Pang Peter Department of Physiology, University of Alberta, T6G 2H7, Edmonton, Alberta, Canada aut NATIONALLICENCE 773 0- Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 345/4(1992-04-01), 478-484 0028-1298 345:4<478 1992 345 210 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer