The Interrelations between the Transport of Sodium and Calcium in Mitochondria of Various Mammalian Tissues

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Abstract
Addition of ruthenium red to mitochondria isolated from brain [rat], adrenal cortex [bovine], parotid gland [bovine] and skeletal muscle [rabbit] inhibits the further uptake of Ca2+ by these mitochondria, but induced little or no net Ca2+ efflux; the further addition of Na+ induces rapid efflux of Ca2+. The velocity of the Na+-induced efflux of Ca2+ from these mitochondria exhibits a sigmoidal dependence on the [Na+]. Addition of Na+ to mitochondria exhibiting the most active Na+-dependent efflux of Ca2+ (brain and adrenal cortex) also releases Ca2+ in the absence of ruthenium red and, under these conditions, the mitochondria became uncoupled. The efflux of Ca2+ from these mitochondria probably occurs via a Na+-dependent pathway, possibly a Na+-Ca2+ antiporter, that is distinct from the ruthenium-red-sensitive carrier that catalyzes energy-linked Ca2+ influx. The possible role of the Na+-dependent efflux process in the distribution of Ca2+ between the mitochondria and the cytosol is discussed. Mitochondria from liver [rat], kidney [rat], lung [rat], uterus muscle [rat] and ileum muscle [rabbit] exhibit no Na+-dependent efflux of Ca2+.

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