The effects of diltiazem were examined on 45Ca efflux in rat parotid glands. First, we showed that mitochondrial Na+/Ca2+ exchange occurs in rat parotid glands and that diltiazem inhibited the mitochondrial Na(+)-dependent calcium efflux. We also confirmed that in rat parotid gland, diltiazem did not modify calcium movements at plasma membrane level. Secondly, we tested the effects of diltiazem on pieces of parotid glands. Diltiazem alone induced 45Ca efflux from parotid lobules. When the effect of diltiazem was tested on isoproterenol-induced 45Ca efflux, the effects of the two drugs were less than additive. By comparison, diltiazem did not modify carbachol induced 45Ca efflux. Diltiazem was able to induce calcium efflux from an intracellular calcium pool, which is not the IP3 sensitive one. These data support the previous hypothesis that isoproterenol and carbachol do not mobilize the same calcium pool. Although we did not precisely determine the calcium pool sensitive to beta-adrenergic stimulation, we cannot rule out the hypothesis that mitochondria would be that store.
Calcium loading of a rat parotid microsomal fraction is greatly increased by an ATP-regenerating system (phosphocreatine and creatine phosphokinase). This effect is neither a consequence of a rise in the ATP concentration nor of an increased formation of inorganic phosphate originating from hydrolysis of ATP or phosphocreatine. Addition of ADP to the incubation medium provokes an inhibition of Ca2+ influx and a stimulation of Ca2+ efflux by the microsomal fraction. These results suggest that the stimulation of Ca2+ uptake by the ATP-regenerating system is due, at least in part, to an increase of Ca2+ influx and a slowing down of Ca2+ efflux as consequence of a decrease of ADP availability. It is proposed that the effect of ADP on Ca2+ movements could account for the action of certain agonists on intracellular Ca2+ concentration. Moreover, the InsP3 responsive Ca2+ pool was also shown to be enlarged by the ATP-regenerating system without modification of InsP3 sensitivity.
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