Chronic nitrite treatment activates adenosine monophosphate-activated protein kinase-endothelial nitric oxide synthase pathway in human aortic endothelial cells

Endothelial dysfunction, with impaired bioavailability and/or bioactivity of the vasoprotective molecule, nitric oxide, appears to be a vital step in initiation atherosclerosis. Several studies have shown that dietary nitrate/nitrite can significant benefits on human cardiovascular homeostasis. Although serum nitrite concentrations reach micromolar levels, physiological significance normal tissues has not been fully elucidated. We investigated vitro chronic effects endothelial oxide synthase (eNOS) determine potential and underlying molecular mechanisms. Our results demonstrate expression phosphorylated eNOS at Ser1177 adenosine monophosphate activated protein kinase (AMPK) Thr172 aortic cells were increased after treatment. suggest stimulation may enhance activation, which is due, part, AMPK activation. The AMPK–eNOS activation by possible mechanism vascular protective nitrate.