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. 2015 Sep 20;23(9):711–723. doi: 10.1089/ars.2014.6059

FIG. 3.

FIG. 3.

Role of C101A-eNOS as a source of increased vascular oxidative stress in C101A/eNOS-KO. Increased (A) aortic and (B) myocardial basal superoxide production in C101A/eNOS-KO, eNOS-KO, and C57BL/6. The cumulative counts/mg of dried tissue measured during incubation with 5 μM lucigenin are given (*p<0.05, two-way ANOVA, n=6–13). (C) Effect of NOS inhibition (L-NAME, 1 mM) on aortic and (D) myocardial superoxide production assessed by lucigenin chemiluminescence in C101A/eNOS-KO, eNOS-KO, and C57BL/6. Results are expressed as counts/tissue dry weight/min (mean±SEM) averaged over the last 8 min of measurement (*p<0.05 vs. all other conditions, one-way ANOVA, n=5–8). (E) Aortic and (F) myocardial nitrotyrosine levels before and after oral treatment with the NO synthase inhibitor, L-NA, in eNOS-KO and C101A/eNOS-KO. Results are given as mean±SEM percentage relative to eNOS-KO (upper panel, *p<0.05 vs. eNOS-KO, one-way ANOVA, n=5–11). The middle panel shows a representative Western blot for protein nitrotyrosine residues, the lower panel shows β-actin expression as loading control. L-NA, Nω-nitro-L-arginine; L-NAME, NG-nitro-L-arginine methyl ester.