Research Paper Volume 15, Issue 19 pp 9913—9947

Figure 4. Effect of aging and reduced DNA double-strand break repair on oxidative stress-mediated suppression of vasodilation. (A) mesenteric artery dose-response curves to increasing doses of the endothelium-dependent vasodilator acetylcholine in the absence and presence of the superoxide scavenger TEMPOL. N = 7–11 per group. (B) Maximal acetylcholine (ACh) vasodilation in mesenteric arteries in the absence and presence of TEMPOL. N = 7–11 per group. (C) Mesenteric artery dose-response curves to increasing doses of the endothelium-dependent vasodilator acetylcholine in the absence and presence of the superoxide scavenger TEMPOL. N = 6–11 per group. (D) Maximal acetylcholine (ACh) vasodilation in mesenteric arteries in the absence and presence of TEMPOL. N = 6–11 per group. (E) Carotid artery superoxide production measured via electron paramagnetic resonance spectrometry. N = 6–8 per group. Individual data points with black borders denote female mice. Individual data points matching group colors denote male mice. ^$p < 0.05 vs. Old ATM +/+ Acetylcholine dose-response curve in the absence of TEMPOL, ^†p < 0.05 vs. Acetylcholine dose-response curve in the presence of TEMPOL from the same group, ^#p < 0.05 vs. Old ATM+/+ Acetylcholine dose-response curve in the presence of TEMPOL, ^*p < 0.05, ^***p < 0.001.