NA-DEPENDENT RELEASE OF INTRACELLULAR CA2+ INDUCED BY PURINOCEPTORS IN PAROTID ACINAR-CELLS OF THE RAT()

In rat parotid acinar cells, ATP caused a transient increase in the in tracellular Ca2+ concentration ([Ca2+](i)) in the absence of external Ca2+. The ATP-induced Ca2+ response was strongly suppressed by removal of external Na+. The sequence of potency in increasing [Ca2+](i) was 3'-o-(4-benzoyl) benzoyl-ATP > ATP > uridine 5'-triphosphate (UTP). Ad enosine, AMP, ADP or alpha,beta-metylene ATP did not cause an increase in [Ca2+](i). The 3'-o-(4-benzoyl) benzoyl-ATP-induced increase in [C a2+](i) was abolished by removal of external Na+, but the UTP-induced response was not. The threshold external Na+ concentration required fo r ATP- or 3'-o-(4-benzoyl) benzoyl-ATP-induced Ca2+ release was 10-20 mM. ATP but not UTP caused a rise in the intracellular Na+ concentrati on ([Na+](i)). Ca2+ release stimulated by caffeine or treatment with r yanodine reduced the Ca2+ release evoked by ATP. These results suggest that ATP, acting through P-2Z purinoceptors, causes Na+ entry by open ing cation-permeable channels, and thereafter the increase in [Na+](i) triggers Ca2+ release from ryanodine-sensitive stores. UTP, acting th rough P-2U purinoceptors, causes Ca2+ release independent of external Na+. (C) 1997 Elsevier Science B.V.