Fig. 2.

Cyp1b1 gene disruption or castration reduced endothelial dysfunction associated with angiotensin (Ang) II-induced hypertension, which was restored by 6β-hydroxytestosterone 6β-OHT. Mice were infused with either Ang II (700 ng/kg/day) or vehicle for 14 days and given i.p. injections of 6β-OHT (15 μg/g b.w every third day) or its vehicle. Endothelial function was measured in the thoracic aorta, as described in the “Materials and methods” section (a–d). Vascular response to increasing concentrations of acetylcholine (ACh; endothelium-dependent relaxation) and sodium nitroprusside (SNP; endothelium-independent relaxation), respectively. *P < 0.05 vehicle, 6β-OHT, Cas+6β-OHT vs. corresponding values from Ang II-treated animals; ^†P < 0.05 Cyp1b1^+/+ Ang II vs. Cyp1b1^−/− Ang II (n = 4 for all experiments, unpaired t test; data are expressed as mean ± SEM)