ATP-PI AND ITP-PI EXCHANGE BY CARDIAC SARCOPLASMIC-RETICULUM

ATP-Pi and ITP-Pi exchange is demonstrated in cardiac sarcoplasmic reticulum isolated from dogs. Both reactions require calcium outside the sarcoplasmic reticulum and inside, as well as magnesium and ADP or IDP. ATP-Pi or ITP-Pi exchange by sarcoplasmic reticulum is maximally activated at μM concentrations of calcium outside the sarcoplasmic reticulum, considerably inhibited by mM concentrations of calcium in the medium and abolished at nM concentrations of calcium in the medium; these last concentrations do not activate phosphorylation of the calcium transport ATPase by ATP or ITP. Phospholipase A-treated sarcoplasmic reticulum vesicles do not exhibit any nucleoside triphosphate-Pi exchange at calcium concentrations between 0.01 and 0.3 mM, but both reactions are partially activated by mM calcium concentrations, indicating that calcium in the mM range inside the sarcoplasmic reticulum is essential for nucleoside triphosphate-Pi exchange. Drugs like prenylamine, chlorpromazine, quinidine, tetracaine and dibucaine inhibit ATP-Pi exchange and calcium-dependent ATPase to a similar extent. Inhibitors of mitochondrial ATP-Pi exchange do not affect ATP-Pi exchange by sarcoplasmic reticulum; dicyclohexyl carbodiimide was an exception in causing increased rate of phosphate exchange in sarcoplasmic reticulum. It is suggested that nucleoside triphosphate-Pi exchange occurs via an exchange of inorganic phosphate with the phosphate of the phosphoprotein formed from nucleoside triphosphate, which is dephosphorylated by nucleoside diphosphate, resulting in ATP or ITP formation. © 1979.