Rat mast cells permeabilized with Sendai virus secrete histamine in response to Ca2+ buffered in the micromolar range

Abstract

In the presence of low extracellular Ca2+, Sendai virus generates permeability lesions in the membrane of rat mast cells. This causes leakage of intracellular phosphorylated metabolites and lactate dehydrogenase; it also permits uptake of normally impermeant aqueous solutes such as the complex of Ca2+ with N-hydroxyethylethylenediaminetriacetic acid. This system was used to buffer the concentration of cytosol Ca2+ in the micromolar range and caused release of the contents of the secretory granules such as histamine and .beta.-N-acetylglucosaminidase. Such release appears to occur by a normal exocytotic secretory mechanism for the following reasons. While leakage of cytosol components is progressively inhibited by Ca2+ in the range 1-10 .mu.M, release of histamine is dependent on Ca2+ in this range. Higher concentrations of Ca2+ are inhibitory to both permeabilization and histamine release. While leakage of phosphorylated metabolites is enhanced in metabolically inhibited cells and the leakage of lactate dehydrogenase is insensitive to metabolic inhibition, the release of histamine and .beta.-N-acetylglucosaminidase is strictly dependent on an intact metabolic process.