NOS3 and hypertensive disorder: This contrasts with the eNOS knockout mice where all functions of eNOS (ie, both NO and reactive oxygen species generation) are deleted, and where there is marked prepregnancy hypertension, but little or no increase in gestational BP.36 Taken together, these findings demonstrate a critical role of endothelial cell BH4 biosynthesis in eNOS regulation in uteroplacental vascular adaptations and BP regulation during pregnancy.