To test this hypothesis, we investigated the contribution of 6β-OHT to the effects of Ang II to increase vascular reactivity, endothelial dysfunction, hypertrophy, fibrosis, and ROS production in Ang II-induced hypertension in the thoracic aorta of castrated Cyp1b1+/+ and Cyp1b1−/− mice that lack endogenous testosterone and 6β-OHT. This evidence concerns the gene CYP1B1 and endothelial dysfunction.