The uptake and release of calcium by heart mitochondria

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Abstract
The kinetics of uptake of Ca2+ by rat heart mitochondria were studied by a spectrophotometric method with Arsenazo III indicator. The exponential rate coefficients measured with or without added phosphate increase with the amount of Ca2+ added up to about 24 .mu.M. Evidence is given that the effect is attributable to a combination of formation of chelates at low concentrations to act as Ca2+ buffers, with co-transport of substrate to provide more respiratory fuel. The inhibitory effect of Mg2+ depends on the Ca2+ concentration, so with a constant [Mg2+]the low concentrations of Ca2+ are most inhibited, and the rate coefficients are still more Ca2+-dependent. Ca2+ uptake is slowed by local anesthetics such as butacaine and dibucaine, and by propranolol and palmitoyl-CoA. After an uptake the release of Ca2+ was investigated. The spontaneous release involves an initially slow and small appearance of free Ca2+ and is followed by an auto-accelerated phase. The release is accompanied by a gradual decrease in internal ATP; it is initiated by palmitoyl-CoA (reversed by carnitine), lysophosphatidylcholine, Na+ salts (reversed by oligomycin) and by K+ salts added to a K+-free medium containing valinomycin. The process is probably a response to an increased energy load imposed on the mitochondria by the various conditions, which include the spontaneous action of phospholipase activated by traces of Ca2+. The problem of how much mitochondrial activity is participating in normal heart Ca2+ turnover is discussed, and experiments showing only 7-14% exchange of the mitochondrial Ca2+ occurring in vivo in 10 or 20 min are reported.