The mechanism by which 6β-OHT mediates the effects of Ang II to increase vascular reactivity and to cause endothelial dysfunction, hypertrophy, and aortic fibrosis in intact Cyp1b1−/− and castrated Cyp1b1+/+ and Cyp1b1−/− mice could be the consequence of the restoration of Ang II-induced increase in BP [16]. Here, CYP1B1 is linked to endothelial dysfunction.