title: An attempt to quantify K+ fluxes in rat liver mitochondria.
abstract: K+ homeostasis in mitochondria is maintained by concerted action of the electrophoretic K+ uniport, driven by the membrane potential, and the electroneutral K+/H+ exchange, driven by [K+] and [H+] gradients. Knowing the driving forces of both pathways and the magnitude of net K+ fluxes under various conditions in rat liver mitochondria suspended in isotonic sucrose medium it was possible to evaluate corresponding rate constants. The rate constant for the K+ uniport under energized conditions was calculated as 0.11 nmol x min-1 x mV-1 x mg protein-1 and that of the antiport was about ten times lower. Activation of the exchanger by depletion of mitochondrial Mg2+ with the ionophore A23187 resulted in an almost tenfold increase of its rate constant, approaching that of the uniport. Quinine and Mg2+ inhibited both K+ transport pathways, whereas glibenclamide, blocker of the ATP-sensitive K+ channel, inhibited the uniport only. The uniport was activated by K+ channel opener P1060.
authors.affiliation: Nencki Institute of Experimental Biology, Warsaw, Poland.
authors.forename: E A
authors.initials: EA
authors.lastname: Belyaeva
authors.forename: L
authors.initials: L
authors.lastname: Wojtczak
mesh_terms: D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D066298:In Vitro Techniques; D007700:Kinetics; D008274:Magnesium / Q000378:metabolism / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D011803:Quinine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D015221:Potassium Channels; D000001:Calcimycin; D011803:Quinine; D008274:Magnesium; D011188:Potassium; D005905:Glyburide