Potentiation by stannous chloride of calcium entry into osteoblastic MC3T3-E1 cells through voltage-dependent L-type calcium channels

The present study was undertaken to confirm that L-type Ca2+ channels are involved in Ca2+ entry into osteoblastic MC3T3-E1 cells and to examine the effect of SnCl2, a Ca2+-channel activator, on the intracellular Ca2+ concentration ([Ca2+](i)). High K+ concentration-dependently raised the [Ca2+](i). All of the L-type Ca2+ channel blockers used here, such as nifedipine, nicardipine, verapamil, and diltiazem, and CdCl2 (a non-selective blocker) inhibited the high K+-induced [Ca2+](i) rise, but omega -conotoxin GVIA (an N-type blocker) and NiCl2 (a T-type blocker) had no effect. Application of SnCl2 alone did not change the [Ca2+](i). However, in the presence of high K+, SnCl2 enhanced the high K+-induced [Ca2+](i) rise, which was inhibited by Ca2+-free medium or nifedipine. In the case where high K+ was applied prior to SnCl2, SnCl2, alone raised the [Ca2+](i) by itself. In conclusion, MC3T3-E1 cells possess the voltage-dependent L-type Ca2+ channels and SnCl2 facilitates the Ca2+ entry through the L-type ones under the condition of the membrane depolarization. There is the possibility that Ca2+ release from intracellular Ca2+ stores is involved in the action of SnCl2. (C) 2001 Harcourt Publishers Ltd.