Transmembrane sodium and potassium gradients modulate histamine secretion induced by ionophore A23187

Abstract

1 Histamine secretion was induced from rat peritoneal mast cells by calcium ionophore A23 187 in the presence of various extracellular calcium concentrations. Transmembrane sodium and potassium gradients were altered by cold pretreatment of mast cells or through the inhibition of sodiumpotassium ATPase by the use of ouabain or potassium-deprivation. 2 Such pretreatments led to a parallel shift to the left of the extracellular calcium concentrationhistamine secretion curve, i.e. to an apparent decrease of extracellular calcium requirement for the ionophore-induced histamine release. 3 These effects were fully reversed by warming mast cells, by washing out ouabain or by adding potassium. Metabolic inhibition of mast cells prevented the ionophore-induced secretion in all the experimental conditions described. Secretion observed in the absence of added calcium was inhibited by short term treatment of cells with 5 x 10-6 M EGTA or EDTA provided magnesium was absent from the assay medium. 4 Data show that ionophore A23187 was able to induce secretion in the presence of micromolar concentrations of extracellular calcium, when the efficiency of the ionophore was not decreased by extracellular m"gnesium and when transmembrane sodium and potassium gradients were altered.

Mechanism of histamine secretion from rat mast cell by calcium reintroduction.

“…On the other hand, it has to be kept in mind that the same treatment inhibiting Na pumping activity potentiates the response to antigen, compound 48/80 or A 23187 (FROSSARD et al, 1983;AMELLAL et al, 1984AMELLAL et al, , 1985. We also confirmed that the same treatment potentiated the response to 48/80 in the presence of EGTA (1 mM), which utilized membrane Ca stores (DOUGLAS and UYEDA, 1973;GARLAND and PAYNE, 1979;PEARCE, 1982).…”

Mast cell activation involves plasma membrane potential‐ and thapsigargin‐sensitive intracellular calcium pools

“…For this latter possibility, experiments shown in figure 2 were carried out in the absence of added Ca2+, ie, free [Ca2+] in the buffer can be considered as approximately 10 p M (Amellal et at, 1985). Therefore, adding 50pM of EGTA allowed to work in the absence of free extracellular Ca2+.…”

“…Histamine release can be observed in the absence of extracellular Ca2+ (Ennis et al, 1980) provided that the stimulus is applied early after CaZ+-deprivation (Lindau and Fernandez, 1986;Bronner ef al, 1987). Indeed, longer pre-incubation of mast cells in a Caz+-free medium leads to a decrease in mast cell responsiveness to a variety of stimuli (Frossard et d, 1983;Amellal et al, 1984Amellal et al, , 1985Lindau and Fernandez, 1986;Bueb et al, 1990a), including the antigen and the classical mast cell activator of the peptidergic pathway, compound 48/80. Cell responsiveness can be restored by the addition of Ca2+, suggesting the involvement of an extracellular Ca2+ source via an as yet unknown process.…”

Na+‐K + pump activity in rat peritoneal mast cells: inhibition by extracellular calcium

“…The secretory response of a number of tissues is enhanced by digitalis glycosides (see references in Amellal et al, 1985), that inhibit the Na'-K' pump activity (Schatzmann, 1953;Skou, 1957;1965;1986;Glynn & Karlish, 1975). However, there are conflicting results concerning the effect of ouabain on the secretion of histamine from rat mast cells and human basophil leucocytes.…”