Figure 1. Time-dependent regulation of superoxide anion and nitric oxide generation by laminar shear stress in human endothelial cells.

Human endothelial cells were exposed to laminar shear stress (ss, 30 dyne cm⁻²) for 2, 8, or 24 h. Superoxide dismutase- and catalase-inhibited superoxide anion (·O₂⁻) formation was determined by cytochrome c reduction assay (A). Release of nitrite, the major metabolite of NO in aqueous solution, was measured using the Griess reaction (B). Impact of NADPH oxidase inhibitor gp91ds-tat (100 μmol l⁻¹) on formation of reactive oxygen species in response to short-term shear stress (ss, 2 h, 30 dyne cm⁻²) was determined by cytochrome c assay. Samples were normalized to internal controls without or with shear stress containing a peptide with a scrambled gp91 sequence (scramb-tat) at the same concentration (C). Values are given as means ±s.e.m. as a percentage of control; n ≥ 3 each; *P < 0.05 versus control.