ARACHIDONIC-ACID ACTIVATES THE NONCAPACITATIVE ENTRY OF CA2+ DURING [CA2+](I) OSCILLATIONS

Current models for agonist-activated Ca2+ entry in nonexcitable cells focus on the capacitative mechanism where entry is activated as a down stream result of the sustained depletion of agonist-sensitive stores w ithout any direct requirement for inositol phosphates. This mechanism has been shown to be important for the sustained Ca2+ signals seen in a variety of nonexcitable cells under conditions of maximal stimulatio n. In contrast, relatively little attention has been given to Ca2+ ent ry under more physiological levels of agonist where, for example, osci llating Ca2+ responses are common. In recent studies using cells from the exocrine avian nasal gland, we have shown that agonist-activated C a2+ entry under these conditions demonstrates properties that are inco nsistent with current versions of the capacitative model. We now repor t that activation of this novel noncapacitative Ca2+ entry is via a di stinct signaling pathway involving an agonist-induced, phospholipase A (2)-mediated generation of arachidonic acid.