[Regulating activity of plasma membranous Ca2+ channels in PC-12 pheochromocytoma cells with chemicals and pharmaceutic agents].

The activity of the voltage-operated Ca2+ channels (VOC channels) and store-operated Ca(2+)-channels (SOC channels) was studied on rat pheochromatocytomic cells PC-12 by using the fluorescence calcium dye Fura-2. The VOC channels were transferred in their open state by depolarizing the plasma membranes of the cells through addition of high KCl concentrations (50 mM). The SOC channels were activated by treating the cells with tapsigargine, a special inhibitor of Ca2+ ATPase in the intracellular Ca2+ stores. Verapamil effectively inhibited the activity of the VOC channels (IC50 = 0.6 micron), but failed to affect the SOC channels. Arachidonic acid reduced the level of [Ca2+]-induced TG (200 nM) at a concentration of 3-10 microns). The movement of Ca2+ along the SOC channels was electrogenic. The depolarization of the plasma membrane of PC-12 cells caused no release of Ca(2+) from the intercellular Ca2+ stores. It is concluded that PC-12 cells are a suitable model to study the activity of different Ca2+ channels and search for chemical compounds that affect the potential-dependent and potential-independent Ca2+ channels.