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Ba2+-induced ATP release from adrenal medullary chromaffin cells is mediated by Ba2+ entry through both voltage- and
1Laboratory of Cell Biology and Genetics, National Institutes of Health, Bethesda, MD 20892.
Abstract:
We have measured on-line the exocytotic secretion of ATP from adrenal medullary chromaffin cells induced by Ba2+ using a luciferin/luciferase assay. We have found that Ba2+-induced ATP release requires the entry of Ba2+ through either voltage- or receptor-gated Ca2+ channels. This conclusion is based on the observations that short preincubations with low concentrations of either nicotine or K+ greatly enhance Ba2+-induced ATP release and that this augmentation can be blocked with the nicotinic receptor antagonist, hexamethonium, and the Ca2+ antagonist, nifedipine, respectively. Moreover, both nicotine and K+ stimulate 133Ba2+ uptake, which in the case of K+ is inhibited by nifedipine. These results support the hypothesis that the cellular events leading to Ba2+-induced secretion coincide at least in part with the events leading to Ca2+-dependent exocytosis.