Early, anti-immunoglobulin induced events prior to NA+-K+pump activation: An analysis in a monoclonal human B-lymphoma cell population

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Abstract
Events following F(ab)2 anti‐δ immunoglobulin stimulation of monoclonal (leukemic) human B cells prior to Na+‐K+ pump activation were investigated in vitro. This pump activation, measured by ouabain‐sensitive 86Rb+ uptake, appeared susceptible to the phospholipid‐interacting drugs tetracaine and quinacrine, to the antioxydant nordihydroguaiaretic acid (NDGA), and to the calmodulin antagonist trifluoperazine, while much less susceptible to the methylation inhibitor‐3‐deazaadenosine. The Ca++ ionophore A 23187 appeared to induce pump activation in a way similar to anti‐δ, as it was susceptible to the same drugs and as anti‐δ had no additional stimulating effect on A 23187‐stimulated cells. However, whereas the anti‐δ‐induced activations appeared independent of the extracellular Ca++ activity, [Ca++]e, the activation by A 23187 was potentiated by addition of the CA++ chelator ethyleneglycol‐bis (β‐aminoethyl ether) N, N'‐tetracetic acid (EGTA). Estimations by a fluorescent chelator method (quin 2) showed anti‐δ to increase the intracellular Ca++ activity, [Ca++]i both in the absence and presence of EGTA. A 23187 increased [Ca++]i strongly in Ca++ medium, but was weaker, more similar to the anti‐δ response, in EGTA medium. It is suggested that Na+‐K+ pump activation after anti‐lg stimulation in B cells may follow Ca++ mobilization from internal stores. The trifluoperazine susceptibility suggests that calmodulin regulation is involved.