Abstract
The effect of nifedipine—an antagonist of L-type calcium (Ca 2+) channels—on capacitative Ca 2+ entry (CCE) was studied in Jurkat T lymphocytes. CCE was induced by a variety of treatments each of which depleted intracellular Ca 2+ stores. Cells were treated with thapsigargin, ionomycin, anti-CD3 antibodies, and phytohaemagglutinin, or pre-incubated in a Ca 2+-free medium. Activity of CCE was evaluated with a Ca 2+-free/Ca 2+-readmission protocol, in Fluo-3 pre-loaded cells. Nifedipine inhibited CCE in a dose-dependent manner. CCE inhibition was not due to non-specific effects on K + channels. Nifedipine, did not induce any membrane depolarization, as revealed by measurements of the plasma membrane potential with the fluorescent probe bis-oxonol. Moreover, experiments done under depolarizing conditions (i.e. by substituting Na + with K + ions in the medium) revealed that nifedipine could inhibit capacitative Ca 2+ entry independently of plasma membrane depolarization. We also demonstrated the presence in our Jurkat T-cells of transcripts for Ca V1.3 (α 1D) and Ca V1.4 (α 1F) L-type Ca 2+ channels. Verapamil and diltiazem, two unrelated blockers of L-type Ca 2+ channels, were less inhibitory on CCE. Possible mechanisms by which nifedipine interferes with Ca 2+ entry in these cells are discussed.
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