Fig. 5
From: High fructose induces dysfunctional vasodilatation via PP2A-mediated eNOS Ser1177 dephosphorylation
Vasodilation function unchanged in the PP2A cKO mice under high fructose stimulation. A Identification of the PP2ACα cKO mice by genotyping. In each group of experiments, the aortic rings were stimulated by fructose (0.25 mM and 2 mM) for 0.5 h, precontracted by using 10–6 M PE, and relaxed by 10–9–10–5 M Ach or SNP. Wire myograph recording the effect of fructose in concentration–response curves to the endothelium-dependent dilator Ach (B) and the endothelium-independent dilator SNP (C) in aortic rings from the PP2ACαflox/flox and cKO mice. D, E The maximal response of Ach and SPN. All data are presented as the mean ± SEM (n = 5 aortic rings). C, control; Fru, fructose; Ach, acetylcholine; SNP, sodium nitroprusside; PE, phenylephrine. *P < 0. 05, **P < 0. 01 when compared with the respective control groups