Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension
J. Clin. Invest. Ulf Landmesser, et al. 111:1201 doi:10.1172/JCI14172 [Go to this article.]

Figure 1
Role of the endothelial NO synthase as a source of ROSs in hypertensive vessels. (a) Effect of endothelial removal and NO synthase inhibition (L-NAME, 1 mM) on vascular superoxide (O₂^•–) production estimated by lucigenin chemiluminescence in sham-operated and DOCA-salt–hypertensive rats (n = 6–10 per group). (b) Vascular O₂^•– production estimated by lucigenin chemiluminescence in sham-operated and DOCA-salt–hypertensive wild-type (C57BL/6), eNOS^–/–, and nNOS^–/– knockout mice (n = 6–10 per group). (c) Vascular O₂^•– production measured by the SOD-inhibitable cytochrome c reduction assay in sham-operated and DOCA-salt–hypertensive wild-type, eNOS^–/–, and nNOS^–/– knockout mice (n = 5–13 per group).