Intracellular Ca2+ buffering potentiates an 86Rb+ permeability response in human lymphocytes.

The effects of antibodies against immunoglobulin delta-heavy chains (anti-delta) on intracellular free Ca2+ concentrations, [Ca2+]i, and 86Rb+ influx in human neoplastic B-cells were tested in vitro. When preloading the cells with high concentrations of the fluorescent Ca2+ chelator quin 2 and subsequently stimulating in EGTA medium, the anti-delta induced rise in [Ca2+]i was strongly reduced or blocked. Nevertheless, 86Rb+ influx, also induced by anti-delta, was potentiated. In fact, in a population of cells in which anti-delta increased [Ca2+]i, but not 86Rb+ influx under standard conditions, the combination of quin-2 preloading and subsequent extracellular Ca2+ chelation by EGTA revealed an anti-delta induced 86Rb+ influx. Most of this influx was ouabain resistant, suggesting only a minor contribution from the Na+/K+ pump. Based on the Ca2+ buffer effect of quin 2 we suggest that the Ca2+ effect on 86Rb+ (K+ analogue) permeability is not mediated by increased [Ca2+]i but rather by the Ca2+ release per se from the plasma membrane.