In spontaneously hypertensive rats (SHR strain), enhanced CYP1B1 activity is associated with left ventricular hypertrophy, whereas the inhibition of CYP1B1 attenuates the increase in blood pressure and limits such manifestations as elevated vascular reactivity, endothelial and renal dysfunction, and fibrosis [29,46] concurrently with a decrease in reactive oxygen species production and in NADPH oxidase activity and increased plasma concentrations of proinflammatory cytokines and catecholamines and enhanced activities of cardiac p38 MAPK, ERK, tyrosine kinase c-Src, and Akt [29]. This evidence concerns the gene AKT1 and left ventricular hypertrophy.