ON THE MECHANISM OF REBOUNDING OF CALCIUM IN LIVER-MITOCHONDRIA

Rat liver mitochondria are able to temporarily lower the steady state concentration of external Ca2+ after having accumulated a pulse of add ed Ca2+. This could be due to inhibition of efflux or/and stimulation of influx of Ca2+. This question has been addressed in mitochondria re spiring on succinate +/- malonate. In the presence of malonate the dep ression of the membrane potential during Ca2+ uptake is more extensive and the rate of Ca2+ uptake slower. There were no discernible differe nces in the rates of efflux either after inhibition of the calcium uni porter by Ruthenium Red or by studying efflux of preloaded Ca-45-label ed Ca2+. The efflux was not changed by diltiazem or cyclosporin A to i nhibit Ca2+ exchange on the Ca2+/nNA(+) antiporter or efflux through t he permeability transition pore. It is concluded that the rebounding i s due mainly to stimulation of the calcium uniporter.