These results suggest that alterations in the systemic 20-HETE biosynthesis represent another time-dependent effect in Ang II hypertensive mice [17] and occur at the stage of significant impairment of systemic NO bioavailability, indicating that 20-HETE pathway could contribute to advanced phase of endothelial dysfunction associated with a systemic fall in NO bioavailability. This evidence concerns the gene AGT and endothelial dysfunction.