The membrane potential of Ehrlich ascites tumor cells: An evaluation of the null point method

The effects of valinomycin (25 pM) on the membrane potential and on initial, passive Na + and K + movements have been determined in Ehrlich ascites tumor cells. The membrane potential of steady‐state cells in a physiologic environment was – 23.2 mV. Addition of valinomycin induced a small, significant hyperpolarization (V m = –29.6 mV) when averaged over the population tested. However, analyses of the response of individual cells to valinomycin showed two different potential effects: (1) the majority of cells hyperpolarized after treatment; but (2) a significant fraction depolarized when exposed to valinomycin. The V m of steady‐state cells incubated in saline with K + at concentrations of 21 mM or 75 mM was – 21.4 mV and –22.0 mV, respectively. Addition of valinomycin to these cells was without effect on V m , thus establishing the “null point” responses. Only for cells incubated in saline with a K + of 75 mM was there agreement between V m and K + equilibrium potential (V k ). Determinations of cellular Na + and K + showed that valinomycin induced net losses of K + and gains of Na + by cells incubated in either physiologic saline or saline with a K + concentration of 21 mM. However, the celular K + of cells incubated in saline with a K + concentration of 75 mM was unaltered by valinomycin. There was a two‐ to threefold increase in K + permeability of the cell membrane in the presence of valinomycin. These results are consistent with the existence of two null points in the membrane‐potential response to valinomycin: One is established when the membrane potential corresponds to V k ; the second occurs when the effects of valinomycin on K + loss from the cell are exactly offset by its inhibition of active Na + + K + transport.