NCF1 and hypertensive disorder: Another example for indirect proof of an uncoupled eNOS was reported in the animal model of deoxycorticosterone acetate salt hypertension (Landmesser et al, 2003), showing the impaired •NO synthesis by a decreased EPR-NO-signal and the increase of eNOS activity in response to supplementation with BH4 or by genetic deletion of the NADPH oxidase subunit p47phox (removing the “kindling radical” for NOS uncoupling).