Transport and metabolism of choline in synaptosomes: energy requirement.

The efflux of Ca2+ from both cardiac and skeletal-muscle mitochondria loaded with 25 nmol of Caz+/mg of protein into a salt-free medium is shown in the form of an Arrhenius plot in Fig. 1. Basal efflux of Caz+ from cardiac and muscle mitochondria increases as the temperature is raised from 17 to 41OC; the respective activation energies are 53 and 87kJ/mol. Between 17 and 34OC Na+-stimulated efflux of Ca2+ appeared to be only slightly dependent on temperature, as indicated by the low activation of 12 and llkJ/mol. At 37 and 4 l o C , Na+-stimulated efflux from muscle mitochondria decreased dramatically compared with the efflux from cardiac mitochondria. Thus cardiac mitochondria seem to be able to resist increased temperature better than skeletal-muscle mitochondria. In the latter case there is an inverse relationship between basal and Na+-stimulated Ca2+ efflux at the higher temperatures. The ability of Na+ to stimulate Ca2+ efflux appears to be contingent upon there being a low basal Ca2+ efflux. Even at low temperatures when the basal efflux has been stimulated, for example by thyroid hormone, the Na+-stimulated etlux is diminished. Increased intracellular Na+ could therefore initiate aerobic mitochondrial Ca2+ cycling in malignant-hyperthermiasusceptible muscle. But as the temperature increased Ca2+ cycling would become independent of the concentration of Na+.