Indeed, several reports have demonstrated that Ang II can lead to eNOS uncoupling by eNOS-glutathionylation, independent of BH4 levels, in several experimental models of hypertension.36,37 In addition, it is possible that the increased blood pressure in response to Ang II may contribute to the development of AAA pathology in Gch1fl/flTie2cre mice. This evidence concerns the gene AGT and Hypertension.