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(Received for publication, April 24, 1996, and in revised form, June 10, 1996)
From the Department of Pharmacology and Physiology, University of
Rochester School of Medicine and Dentistry,
Rochester, New York 14642
Current models for agonist-activated
Ca2+ entry in nonexcitable cells focus on the capacitative
mechanism where entry is activated as a downstream result of the
sustained depletion of agonist-sensitive stores without 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 stimulation.
In contrast, relatively little attention has been given to
Ca2+ entry under more physiological levels of agonist
where, for example, oscillating Ca2+ responses are common.
In recent studies using cells from the exocrine avian nasal gland, we
have shown that agonist-activated Ca2+ entry under these
conditions demonstrates properties that are inconsistent with current
versions of the capacitative model. We now report that activation of
this novel noncapacitative Ca2+ entry is via a distinct
signaling pathway involving an agonist-induced, phospholipase
A2-mediated generation of arachidonic acid.
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