Amiloride inhibits anti-Ig induction of proliferation in a human B-lymphoma cell population.
The effects of amiloride on increased 86Rb+ influx, an early event of lymphocyte activation, and on the late event, [3H]thymidine uptake, were compared in anti-Ig-stimulated human B-lymphoma cells in vitro. Both events were inhibited to significant and comparable extents, and the drug effects were apparently not due to unspecific toxicity. This suggests that the increased 86Rb+ influx reflects early changes (e.g. amiloride-sensitive Na+-H+ exchange) which are required for anti-Ig induction of B-lymphocyte proliferation.
D000584:Amiloride / Q000494:pharmacology*; D000888:Antibodies, Anti-Idiotypic / Q000502:physiology*; D001402:B-Lymphocytes / Q000187:drug effects* / Q000378:metabolism; D001692:Biological Transport / Q000187:drug effects; D004247:DNA / Q000096:biosynthesis; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects*; D008223:Lymphoma / Q000097:blood*; D011719:Pyrazines / Q000494:pharmacology*; D012413:Rubidium / Q000097:blood; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013936:Thymidine / Q000378:metabolism
D000888:Antibodies, Anti-Idiotypic; D011719:Pyrazines; D000584:Amiloride; D004247:DNA; D012413:Rubidium; D013755:Tetradecanoylphorbol Acetate; D013936:Thymidine