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Arachidonic acid regulates two Ca2+ entry pathways via nitric oxide.
Eileen L Watson1, Kerry L Jacobson, Jean C Singh
1Department of Oral Biology, University of Washington, Seattle, WA 98195, USA. ewatson@u.washington.edu
Cellular Signalling
|November 26, 2003
Summary
Arachidonic acid (AA) modulates calcium (Ca2+) entry in mouse parotid acini. AA inhibits capacitative Ca2+ entry (CCE) while activating a distinct pathway linked to ryanodine-sensitive stores via nitric oxide.
Area of Science:
- Cellular Physiology
- Ion Channels
- Signal Transduction
Background:
- Capacitative Ca2+ entry (CCE) is a well-characterized Ca2+ influx pathway.
- Arachidonic acid (AA) is implicated in regulating cellular processes, including ion transport.
Purpose of the Study:
- To investigate the effects of arachidonic acid (AA) on Ca2+ entry pathways in mouse parotid acini.
- To elucidate the mechanisms underlying AA-regulated Ca2+ influx and its interaction with CCE.
Main Methods:
- Measurement of intracellular Ca2+ concentrations in response to AA.
- Pharmacological manipulation of Ca2+ stores and entry pathways using thapsigargin (Tg), gadolinium (Gd3+), tetracaine, and nitric oxide synthase (NOS) inhibitors.
- Utilized a nitric oxide (NO) donor (GEA 3162) to assess NO's role.
Main Results:
- AA induced Ca2+ release from intracellular stores and increased Ca2+ entry.
- AA inhibited thapsigargin-induced CCE but activated Ca2+ entry when CCE was blocked.
- AA-induced Ca2+ entry and release were sensitive to tetracaine and NOS inhibition (7-NI).
- The NO donor GEA 3162 mimicked AA's inhibition of CCE.
Conclusions:
- Arachidonic acid (AA) differentially regulates Ca2+ entry pathways in mouse parotid acini.
- AA inhibits the Ca2+-selective CCE pathway and activates a separate Ca2+ entry pathway dependent on ryanodine-sensitive stores.
- Nitric oxide (NO) mediates AA's effects on these Ca2+ entry pathways.