Figure 1.

H₂O₂ increases O₂ ^.‐ production and VSM [Ca^{2 +}]_i but not vasoconstriction in coronary arteries from genetically obese rats. (A, B) Effect of H₂O₂ (10 and 100 μM) and the free radical scavenger tempol (30 μM) on the production of O₂ ^.‐ in coronary artery (A) and in the myocardium (B) of LZR and OZR. (C, D) H₂O₂ induced a contractile effect of similar magnitude in arteries from LZR and OZR in coronary (CA) (C) and mesenteric arteries (MA) (D) precontracted with K⁺30. (E, F) Summarized data showing the changes in [Ca^{2 +}]_i (E) and tension (F) in response to a single dose of H₂O₂ (100 μM) in endothelium‐intact coronary arteries from LZR and OZR. (A, B) Results are expressed as counts min^‐1 mg^‐1 of tissue and represent the mean ± SEM of 8–20 animals. **P < 0.01 versus control before treatment; ##P < 0.01 versus H₂O₂‐treated; †P < 0.05, ††P < 0.01 versus LZR. (C‐F) Results are expressed either as a percentage of the KPSS‐induced responses (C, D, F) or as absolute values of ratio (E) and represent the mean ± SEM of 5–13 arteries (1–2 per animal). *P < 0.05.