GCH1 and endothelial dysfunction: In many gene transfer animal models of GTPCH-I, such as diabetic GCH-Tg mice and DOCA-salt hypertension rat, overexpression of GTPCH-I could reverse the BH4 deficiency and endothelial dysfunction by reducing superoxide anion production and NO-mediated vasodilatation was preserved [14, 15].