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 Ca2+ 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 Ca2+ 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. (C) 2000 Academic Press.
|Number of pages||5|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Aug 11 2000|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology