Hypotonic stress-induced NO production in endothelium depends on endogenous ATP.
The mechanism by which mechanical stress induces nitric oxide (NO) synthesis in endothelium is still controversial. Hypotonic stress (HTS, -20%) induced ATP release, which evoked Ca(2+) transients in bovine aortic endothelial cells (BAEC). HTS also induced NO synthesis, assessed by DAF-2 fluorescence, which was suppressed by inhibiting endogenous ATP-induced Ca(2+) transients with suramin or neomycin. Exogenously applied ATP mimicked these responses. Pretreatment with wortmannin did not affect DAF-2 fluorescence, suggesting that Akt phosphorylation was not involved in HTS-induced NO synthesis. These results indicate that endogenous ATP plays a central role in HTS-induced NO synthesis in BAEC.
Department of Pharmacology, Kyushu University, Fukuoka, 812-8582, Japan.
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C
Kimura
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Koyama
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Oike
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Ito
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000378:metabolism*; D005453:Fluorescence; D005456:Fluorescent Dyes; D006863:Hydrogen-Ion Concentration; D007038:Hypotonic Solutions; D009569:Nitric Oxide / Q000096:biosynthesis*
D005456:Fluorescent Dyes; D007038:Hypotonic Solutions; D009569:Nitric Oxide; D000255:Adenosine Triphosphate