Relative contributions of mitochondrial and non-mitochondrial oxidative stress in age-related cutaneous microvascular endothelial dysfunction

; 28mM sodium nitroprusside+43°C). Tempol improved the local heating response compared with Ringer's (76.37 ± 18.99 vs. 51.07 ± 23.36, p = 0.02), but MitoTempo (p = 0.25) did not. Likewise, Tempol improved the NO contribution to the response compared with Ringer's (61.40 ± 15.92 vs. 37.02 ± 20.64, p = 0.01), but MitoTempo (p = 0.69) did not. Conversely, MitoTempo increased the non-NO-mediated component of the response compared with Ringer's (13.95 ± 16.43 vs. 4.04 ± 6.14; p < 0.01), but Tempol did not (p = 0.41). There were no differences between Tempol or MitoTempo (p ≥ 0.14). These data suggest that, although mitochondrial oxidative stress may contribute, a considerable portion of the oxidative stress underlying age-related endothelial dysfunction is derived outside of the mitochondria.