Figure 5.

Inhibition of NA‐induced vasoconstriction. (a) Concentration–response curves to NA, obtained in endothelium‐denuded rat aortic rings pre‐incubated with vehicle or erucin at the concentrations of 10, 30, and 100 μM. The effects are expressed as a % of the contractile responses previously induced by the administration of KCl 60 mM. The vertical bars indicate the SEM. Six different experiments were performed, each with six replicates (n = 6). The asterisks indicate a significant difference from the NA‐induced vasoconstriction curve obtained on endothelium‐denuded aortic rings pre‐incubated with the vehicle (*P < 0.05). (b) Representative microdynamometric tracings obtained in two different aortic rings, demonstrating that the inhibitory effects of erucin were fully reversible. In the upper panel, one aortic ring was pre‐incubated with vehicle (20 min); thereafter, cumulative increasing concentrations of NA, evoking concentration‐dependent vasoconstriction, were added. The aortic ring was submitted to washout (W) and adequate equilibration time to recover again the resting tension. Then, the aortic ring was treated again with vehicle (20 min); thereafter, cumulative increasing concentrations of NA, evoking concentration‐dependent vasoconstriction, were added again. In the lower panel, the other aortic ring was pre‐incubated with erucin 100 μM (the highest concentration, for 20 min); thereafter, cumulative increasing concentrations of NA, evoking reduced concentration‐dependent vasoconstriction, were added. The ring was submitted to washout (W) and an adequate equilibration time to recover again the resting tension. Finally, the aortic ring was treated with vehicle (20 min); thereafter, cumulative increasing concentrations of NA, evoking concentration‐dependent vasoconstriction, were added again. In the lower panel, complete recovery of the vasoconstriction effects of NA is evident