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. Author manuscript; available in PMC: 2013 Nov 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2012 Sep 18;264(3):351–360. doi: 10.1016/j.taap.2012.09.007

Figure 3.

Figure 3

Loss of CYP1A1 does not alter vascular sensitivity to ACh- or SNAP-mediated vasodilation, nor PE-mediated contraction in the absence or presence of the NOS inhibitor, LNNA. (A-D) Thoracic aorta and (E) Mesenteric arterioles. (A) ACh-mediated dilation (% PE preconstriction), (B) SNAP-mediated dilation in endothelium denuded aorta (% PE preconstriction), (C) PE-mediated constriction (% KCl), and (D) PE-mediated constriction in the presence of LNNA, (E) ACh-mediated relaxation (% U46619 preconstriction). Data represent mean ± SEM and were analyzed by two-way, repeated measures ANOVA, using post hoc Holm-Sidak comparisons (n=7–8/genotype).