Contribution of prostanoids and other relaxing pathways to the endothelial dysfunction. A: dose–response relaxation curves to acetylcholine (ACh) in Sham (A), non-treated 2K1C hypertensive (B) and sildenafil-treated 2K1C (C) mice. Dose–response curves to ACh were obtained with and without the double blockade of NOS with L-NAME and of cyclooxygenases with indomethacin. Bar graphs show the area under the curve (AUC) after the double blockade (D), the total AUC minus the AUC after the double blockade (contribution of EDHF and other pathways, E) and the AUC derived from the AUC under double blockade minus the AUC under the L-NAME blockade (prostanoids pathway, F). Graphs G and H show the effects of indomethacin on the maximum relaxation (Rmax, G) and sensitivity (pEC50, H) and on these two parameters. Values are the means±SEM for 8 to 10 animals per group. *p < 0.05, #p < 0.05, **p < 0.01and ##p < 0.01, compared with the group indicated by the line; two-way ANOVA (A, B and C) and one-way ANOVA (D-H).