Fig. 1.

Cyp1b1 gene disruption or castration minimized the increase in the aortic response to vasoconstrictor agents associated with angiotensin (Ang) II-induced hypertension, which was restored by 6β-hydroxytestosterone (6β-OHT). Intact or castrated Cyp1b1^+/+ and Cyp1b1^−/− 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. Vascular reactivity was measured in the aorta as described above (a–d). The response of the aorta of intact or castrated Cyp1b1^+/+ and Cyp1b1^−/− mice infused with Ang II and treated with 6β-OHT to increasing concentrations of phenylephrine (PE) and endothelin-1 (ET-1). *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 = 4–5 for all experiments, unpaired t test; data are expressed as mean ± SEM)