Fig. 1.

Differential responses of WT and KI vessels to NO₂-OA. (A) WT or KI mesenteric vessels were constricted with the thromboxane mimetic U46619, and then increasing doses of NO₂-OA were added. The KI vessels showed a significantly impaired relaxation to NO₂-OA as indicated by their dose–response curve being shifted to the right compared with the WT. (B) NO₂-OA–dependent vasorelaxation was nitric oxide independent as the soluble guanylate cyclase inhibitor ODQ did not alter the dose–response curve. (C) sEH activity was assessed in hearts from WT or KI mice that had been implanted with an osmotic pump containing NO₂-OA or saline. NO₂-OA reduced sEH activity in WT but not in KI mice (*P < 0.05 ANOVA with post hoc t test).