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J Biol Chem. 1996 Sep 6;271(36):21720-5.

Arachidonic acid activates the noncapacitative entry of Ca2+ during [Ca2+]i oscillations.

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1
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA.

Abstract

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.

PMID:
8702966
[Indexed for MEDLINE]
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