NO-dependent flow-mediated vasodilatation is reduced in myometrial arteries isolated from hypertensive pregnancies (HTP).10 We have demonstrated that a feature of abnormal eNOS activity in cardiovascular disease states is loss of the required eNOS cofactor, tetrahydrobiopterin (BH4), that is synthesized in endothelial cells by the enzyme GTPCH (GTP cyclohydrolase 1), encoded by GCH1. The gene discussed is NOS3; the disease is cardiovascular disorder.