Figure 6.

Effects of the specific inhibitor Nω-nitro-L-arginine on Ach-induced relaxation in aortas of mice with wild-type/knocked-out CB₁R and LDLR kept on a control or a high-fat diet, normalized to control values. Attenuation of Ach-induced relaxation with LNA is shown in percent values. Panel (A): Attenuation of Ach-induced relaxation with LNA in CB₁R+/+, LDLR+/+, CD and HFD groups, n = 5–10. Panel (B): Attenuation of Ach-induced relaxation with LNA in CB₁R+/+, LDLR−/−, CD and HFD groups, n = 5–7. Panel (C): Attenuation of Ach-induced relaxation with LNA in CB₁R−/−, LDLR+/+, CD and HFD groups, n = 6–9. Panel (D): Attenuation of Ach-induced relaxation with LNA in CB₁R−/−, LDLR−/−, CD and HFD groups, n = 6–7. p-values < 0.05 were considered significant. *, p < 0.05; **, p < 0.01; ***, p < 0.001 between CD and HFD groups in the same genotype (one-way ANOVA with Bonferroni post hoc test). Mean ± SEM values are indicated here, with dots showing individual data points. Abbreviations: CD, control diet; HFD, high-fat diet; LNA, Nω-nitro-L-arginine; CB₁R+/+, cannabinoid type 1 receptor wild type; CB₁R−/−, cannabinoid type 1 receptor knockout; LDLR+/+, LDL receptor wild type; LDLR−/−, LDL receptor knockout. Relaxation data were calculated as percent values of the precontraction level.