ATP induces nucleotide permeability in rat mast cells

Abstract

ATP IS one of several agonists which stimulate Ca²⁺-dependent exocytotic degranulation of mast cells, causing the release of histamine and other mediators of immediate hypersensitivity^1–3. The concentration–effect relationship of ATP on mast cells is characterised by the sharp onset of self-inhibition as the concentration is raised above the optimum for histamine secretion⁴. We have previously shown that stimulation of mast cells with IgE-directed ligands (antigen, concanavalin A), chymotrypsin and compound 48/80 is accompanied by an increased turnover of phosphatidylinositol⁵ similar to that observed for Ca²⁺-mediated responses in other tissues⁶. At concentrations of ATP which cause inhibition we have observed a reduction in phosphatidylinositol turnover to less than control levels (unpublished results). We show here that the inhibition by ATP is correlated with an extensive leakage of phosphorylated metabolites from the cells.