Effects of a switched, time-varying 1.7 T magnetic field on Rb (K ) uptake by HeLa S3 cells incubated in an isosmotic high K medium were examined. The magnetic flux density was varied intermittently from 0.07±1.7 T at an interval of 3 s. K uptake was activated by replacement of normal medium by high K medium. A membrane-permeable Ca 2 chelating agent (BAPTA-AM) and Ca 2 -dependent K channel inhibitors (quinine, charibdotoxin, and iberiotoxin) were found to reduce the Rb (K ) uptake by about 30±40%. Uptake of K that is sensitive to these drugs is possibly mediated by Ca 2 -dependent K channels. The intermittent magnetic field partly suppressed the drug-sensitive K uptake by about 30±40% (P 0X05). To test the mechanism of inhibition by the magnetic fields, intracellular Ca 2 concentration ([Ca 2 ]c) was measured using Fura 2-AM. When cells were placed in the high K medium, [Ca 2 ]c increased to about 1.4 times the original level, but exposure to the magnetic fields completely suppressed the increase (P 0X01). Addition of a Ca 2 ionophore (ionomycin) to the high K medium increased [Ca 2 ]c to the level of control cells, regardless of exposure to the magnetic field. But the inhibition of K uptake by the magnetic fields was not restored by addition of ionomycin. Based on our previous results on magnetic field-induced changes in properties of the cell membrane, these results indicate that exposure to the magnetic fields partly suppresses K influx, which may be mediated by Ca 2dependent K channels. The suppression of K fluxes could relate to a change in electric properties of cell surface and an inhibition of Ca 2 influx mediated by Ca 2 channels of either the cell plasma membrane or the inner vesicular membrane of intracellular Ca 2 stores. Bioelectromagnetics 21:228±237, 2000.