Mitochondrial Ca2+ fluxes and levels during ischaemia and reperfusion: possible mechanisms.
It has been shown that myocardial ischaemia depresses the uptake and enhances the release of Ca2+ by mitochondria. Reperfusion of the ischaemic areas may result in a further deterioration of the above processes. Despite these marked changes in Ca2+ fluxes, reperfusion has been shown always to be associated with a marked increase in mitochondrial Ca2+ content. To explain the latter observation, it has been proposed that reperfusion promotes respiration-supported mitochondrial Ca2+ uptake in preference to ADP phosphorylation. To evaluate this hypothesis, the effect of exogenous ADP on mitochondrial respiration-linked Ca2+ uptake was investigated in control, ischaemic and ischaemic-reperfused hearts. The results show that ADP significantly depresses mitochondrial Ca2+ uptake in all three preparations, indicating that Ca2+ is not taken up preferentially to ADP phosphorylation in reperfused tissue. It is suggested that reperfusion-induced increased mitochondrial Ca2+ levels are probably not due to increased respiration-linked Ca2+ uptake, but rather to augmented conversion of ionized Ca2+ to calcium phosphate which does not participate in ionic fluxes.
D000244:Adenosine Diphosphate / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D010101:Oxygen Consumption; D010477:Perfusion; D010766:Phosphorylation; D051381:Rats; D011919:Rats, Inbred Strains
D000244:Adenosine Diphosphate; D002118:Calcium