TY - JOUR
T1 - The membrane potential of Ehrlich ascites tumor cells
T2 - An evaluation of the null point method
AU - Smith, Thomas C.
AU - Robinson, Susan C.
PY - 1981/3
Y1 - 1981/3
N2 - 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 (Vm = –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 Vm 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 Vm, thus establishing the “null point” responses. Only for cells incubated in saline with a K+ of 75 mM was there agreement between Vm and K+ equilibrium potential (Vk). 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 Vk; 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.
AB - 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 (Vm = –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 Vm 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 Vm, thus establishing the “null point” responses. Only for cells incubated in saline with a K+ of 75 mM was there agreement between Vm and K+ equilibrium potential (Vk). 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 Vk; 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.
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U2 - 10.1002/jcp.1041060309
DO - 10.1002/jcp.1041060309
M3 - Article
C2 - 7217220
AN - SCOPUS:0019418483
VL - 106
SP - 399
EP - 406
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
SN - 0021-9541
IS - 3
ER -