Effects of excessive noradrenaline on cardiac mitochondrial calcium transport and oxidative phosphorylation.

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Abstract
Mitochondrial oxidative phosphorylation, Ca transport activity and Ca content were investigated in dog hearts injured by excessive noradrenaline [norepinephrine] (NA). Diffuse cardiac injury was produced by a 5-h infusion of NA (2 or 5 .mu.g/kg per min), and the injury was evaluated based on ECG and hemodynamic changes. Mitochondrial Ca uptake and binding activities measured in the presence of ATP showed no significant differences between the control and NA groups. However, the Ca content of heart mitochondria isolated from the NA groups, state 3 respiration and the respiratory control index were significantly depressed without any change in the ADP/O ratio. Excessive NA apparently causes the intracellular Ca overload and the depression of mitochondrial respiration, and both of these changes may play a key role in the pathogenesis of myocardial injury through the insufficient control of cytosolic Ca levels.