Regulation of the monovalent cation permeability of brain mitochondria.
The Na+ and K+ conductances of rat brain mitochondria were estimated from rates of metabolically dependent swelling and uncoupling of respiration. These were maximal in the presence of EDTA plus Pi. Pi could not be replaced with acetate. Na+ conductance was greater than that of K+ and was therefore examined in greater detail. According to the influences of N-ethylmaleimide, internal Pi (exogenous and perhaps endogenous) promoted Na+ permeability. Treatment with the ionophore A23187 obviated the Pi requirement although EDTA was still necessary. The stimulation by EDTA with Pi or A23187 and inhibition by exogenous Mg2+ suggested endogenous polyvalent cations could also regulate Na+ conductance. The influence of these substances upon endogenous Mg2+ (and Ca2+) levels is consistent with such a role of membrane-bound Mg2+. Low levels of ruthenium red (150 pmol/mg) inhibit Na+ permeation, indicating that the number of 'sites' or 'channels' involved may be small. The Ca2+ uniport is not directly involved in Na+ flow according to its greater sensitivity to inhibition by ruthenium red.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D001921:Brain / Q000378:metabolism*; D000001:Calcimycin / Q000494:pharmacology; D004492:Edetic Acid / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D010539:Permeability; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012402:Rotenone / Q000494:pharmacology; D012430:Ruthenium Red / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D014634:Valinomycin / Q000494:pharmacology
D012402:Rotenone; D012430:Ruthenium Red; D014634:Valinomycin; D000001:Calcimycin; D004533:Egtazic Acid; D004492:Edetic Acid; D012964:Sodium; D011188:Potassium