Figure 5.

OS in kidneys. Expression of eNOS was highly increased in diabetic animals, suggesting eNOS uncoupling (A). Treatment with Ang-(1–7) reduced levels of eNOS mRNA. Co-administration with A-779, PD123319, L-NAME and icatibant inhibited effects of Ang-(1–7). Level of eNOS phosphorylated on both Ser¹¹⁷⁷ (active form) (B) and Thr⁴⁹⁵ (inactive form) (C) was increased in diabetic animals. Treatment further elevated levels of eNOS phosphorylation at Ser¹¹⁷⁷. Co-administration of A-779 increased levels of this marker. Ang-(1–7) reduced abundance of the deactivated form of eNOS. This effect was reversed after treatment with A-779. Ang-(1–7) decreased nitrotyrosine staining in kidney sections from diabetic animals (D). Co-administration of A-779, PD123319 or L-NAME reversed the effects of Ang-(1–7) on nitrotyrosine formation (Hz – heterozygous; db – diabetic). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. Significantly different compared with db + Ang-(1–7), †P < 0.05; ††P < 0.01; or ††††P < 0.0001; calculated using Kruskal–Wallis (A) or one-way anova (B–D).