Abstract
It has been reported that the synthetic heptapeptide cholecystokinin (CCK) analogue JMV-180 evokes cytosolic Ca2+ signals in pancreatic acinar cells via mechanisms that do not include either the generation or action of inositol 1,4,5-trisphosphate (InsP3) (Saluja, A. K., Dawra, R. K., Lerch, M. M., and Steer, M. L. (1992) J. Biol. Chem. 267, 11202-11207; Yule, D. I., and Williams, J. A. (1992) J. Biol. Chem. 267, 13830-13835). We have now investigated the CCK- and JMV-180-evoked cytosolic Ca2+ oscillations by measurement of the Ca(2+)-sensitive ion currents in internally perfused mouse pancreatic acinar cells. We find that the InsP3 receptor antagonist heparin (500 micrograms/ml) blocks Ca2+ oscillations induced by both CCK (5-20 pM) and JMV 180 (10-40 nM), whereas de-N-sulfated heparin (500 micrograms/ml), which does not affect InsP3 binding to its receptor, fails to inhibit the responses to the two agonists. We conclude that the cytosolic Ca2+ oscillations evoked by both CCK and JMV-180 are dependent on functional InsP3 receptors.
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