Abstract
Depolarization of PC-12 pheochromocytoma cells with K + produces an immediate increase in catecholamine release. The stimulation of release is blocked by Co 2+, removal of extracellular Ca 2+ or by dihydropyridine drugs such as nitrendipine. Release is enhanced by other dihydropyridines such as BAY K8644. Release is accompanied by a voltage dependent uptake of 45Ca 2+ which is also blocked by Co 2+ or nitrendipine and enhanced by BAY K8644. The phorbol ester phorbol 12-myristate-13-acetate (TPA) in the range 10 −9 – 10 −6 M produced little effect by itself but augmented the K + evoked release of catecholamine. An analog of TPA which does not activate protein kinase C was ineffective. In contrast, TPA in the same concentration range blocked influx of 45Ca 2+ induced by 70 mM K + or 70 mM K +/ BAY K8644. 45Ca 2+ influx produced by A23187 was not blocked by TPA. The results suggest a system by which protein kinase C may regulate the output of transmitters from secretory cells.
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