Figure 5.

Contribution of eNOS‐derived H₂O₂ in mouse mesenteric arteries. Isometric tension of second‐order mesenteric arteries from (A) WT and (B) Gch1 ^fl/flTie2cre mesenteric arteries was recorded. Endothelium‐dependent vasodilatation to ACh was determined in the presence of the cyclooxygenase inhibitor, indomethacin (10 μmol·L⁻¹) alone, indomethacin with PEG‐catalase (400 units·mL⁻¹), indomethacin with the NOS inhibitor, L‐NAME (100 μmol·L⁻¹), indomethacin and L‐NAME with PEG‐catalase. Data are expressed as mean ± SEM (n = 8 to 10 animals per group). *P < 0.05, #P < 0.05; significantly different as indicated. (C) Inhibitable‐component, expressed as percentage maximum relaxation in the presence of indomethacin, after treatment of PEG‐catalase, or L‐NAME, or PEG‐catalase with L‐NAME. *P < 0.05, significantly different from WT; #P < 0.05, significantly different from catalase treatment of the same genotype; n = 8 WT and 10 Gch1 ^fl/flTie2cre, one WT mice was re‐genotyped as a Gch1 ^fl/flTie2cre mouse and re‐assigned at the end of the experiment).