Original Contribution Early determinants of H 2 O 2 -induced endothelial dysfunction

Reactive oxygen species (ROS) can stimulate nitric oxide (NO U ) production from the endothelium by transient activation of endothelial nitric oxide synthase (eNOS). With continued or repeated exposure, NO U production is reduced, however. We investigated the early determinants of this decrease in NO U production. Following an initial H2O2 exposure, endothelial cells responded by increasing NO U production measured electrochemically. NO U concentrations peaked by 10 min with a slow reduction over 30 min. The decrease in NO U at 30 min was associated with a