Effects on mitochondrial K flux of pH, K concentration, and N-ethyl maleimide.
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 V max 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 V max 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.
D000818:Animals; D000968:Antimycin A / Q000494:pharmacology; D001693:Biological Transport, Active / Q000187:drug effects; D004140:Dinitrophenols / Q000494:pharmacology; D005033:Ethylmaleimide / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D051381:Rats
D004140:Dinitrophenols; D000968:Antimycin A; D005033:Ethylmaleimide; D011188:Potassium