In non-excitable cells, many agonists increase the intracellular Ca# + concentration ([Ca# + ] i ) by inducing an inositol 1,4,5-trisphosphate (IP $ )-mediated Ca# + release from the intracellular stores. Ca# + influx from the extracellular medium may then sustain the Ca# + signal. [Ca# + ] i recovers its resting level as a consequence of Ca# + -removing mechanisms, i.e. plasma-membrane Ca# + -ATPase (PMCA) pump, Na + \Ca# + exchanger (NCX) and sarco-endoplasmic reticulum Ca# + -ATPase (SERCA) pump. In a study performed in pancreatic acinar cells, evidence has been provided suggesting that, during the decay phase of the agonistevoked Ca# + transients, the Ca# + concentration within the intracellular stores remains essentially constant [Mogami, Tepikin and Petersen (1998) EMBO J. 17, [435][436][437][438][439][440][441][442]. It was therefore hypothesized that, in such a situation, intracellular Ca# + is not only picked up by the SERCA pump, but is also newly released through IP $ -sensitive Ca# + channels, with the balance between these two processes being approximately null. The main aim of the present work was to test this hypothesis by a different experimental approach. Using cardiac microvascular endothelial cells, we found that inhibition of the SERCA pump has no effect on the time course of agonist-evoked Ca# + transients. This

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