Tetrahydrobiopterin-dependent preservation of nitric oxide–mediated endothelial function in diabetes by targeted transgenic GTP–cyclohydrolase I overexpression
J. Clin. Invest. Nicholas J. Alp, et al. 112:725 doi:10.1172/JCI17786 [Go to this article.]

Figure 7
Isometric tension studies in aortic rings from diabetic and control GCH-Tg and WT mice (n = 5–8 animals per group). (a) Vessel relaxations to the endothelium-dependent agonist acetylcholine were normal in control GCH-Tg (filled circles) and WT mice (filled squares). (b) Diabetic WT mice (open squares) exhibited impaired endothelium-dependent relaxations as compared with GCH-Tg mice (open circles) (*P = 0.002) and with control WT mice (filled squares, P = 0.048). There was no difference in endothelium-dependent relaxations between diabetic and control GCH-Tg mice (open and filled circles, respectively; P = 0.468). (c and d) Vessel relaxations to the NO donor sodium nitroprusside were identical in all groups of mice.