Fig. 7

Cyp1b1 gene disruption minimized angiotensin (Ang II)-induced superoxide production, which was reversed by 6β-hydroxytestosterone (6β-OHT). Cyp1b1^+/+ and Cyp1b1^−/− mice were infused with vehicle or Ang II (700 ng/kg/day) (upper panel) and treated with 6β-OHT (15 μg/g b.w every third day) or 6β-OHT+Ang II (lower panel) for 14 days. Aortic superoxide production was determined by the fluorescence intensity of 2-hydoxyethidium (a, b). Photomicrographs are representative of the aorta from mice in each of the different treatment groups following incubation with dihydroethidium. The graph depicts the quantified data. *P < 0.05 vehicle, 6β-OHT vs. corresponding value from Ang II-treated animal; ^†P < 0.05 Cyp1b1^+/+ Ang II vs. Cyp1b1^−/− Ang II (n = 3 for all experiments, unpaired t test; data are expressed as mean ± SEM)