Effects on Mitochondrial K Flux of pH, K Concentration, andN-Ethyl Maleimide

Publisher Website
Google Scholar
Abstract
Based on published evidence that cation transport in mitochondria is not significantly dependent on a membrane potential, it is suggested that the process of mitochondrial cation transport may be nonelectrogenic. These experiments focused on the possibility that K+ flux into rat liver mitochondria may be directly coupled, via an energy-linked carrier mechanism, to OH− influx or H+ efflux. The dependence of the unidirectional K+ influx on the external K+ concentration indicates involvement of a saturable mechanism. Increasing the external pH from 7.0 to 8.0 increases the apparent Vmax of the K+ influx without significantly altering the apparent Km for K+. The pH dependence is greater in the presence of N-ethyl maleimide, a known inhibitor of the mitochondrial Pi/OH− exchange mechanism. N-Ethyl maleimide decreases the apparent Vmax at pH 7.0 and increases it at pH 8.0. Evidence indicates that both N-ethyl maleimide and a high external Pi concentration may stimulate the K+ influx at alkaline external pH (8.0) by preventing net exchanges between endogenous Pi and external OH−. An apparent first-order dependence of the K+ influx on the external OH− concentration is observed in the presence of N-ethyl maleimide. These results are consistent with a possible role of external OH− as a cosubstrate of the K+ transport mechanism.