Ba²⁺-induced atp release from adrenal medullary chromaffin cells is mediated by Ba²⁺ entry through both voltage- and receptor-gated Ca²⁺ channels

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 K²⁺ stimulate ¹³³Ba²⁺ uptake, which in the case of K²⁺ 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.