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. 2009 Feb 6;296(4):H1133–H1140. doi: 10.1152/ajpheart.00929.2008

Fig. 1.

Fig. 1.

Phenylephrine (PE)-mediated vascular contraction in endothelium-intact mouse aortic rings from α-galactosidase A (Gla) wild-type (Gla+/0) and Gla-knockout (Gla−/0) mice in the absence of cyclooxygenase (COX) inhibitor (A) or in the presence of 10−5 mol/l indomethacin (INDO; B), 3 mmol/l valeryl salicylate (VS; C), or 10−6 mol/ NS-398 (D). Data are expressed as percentage of contraction elicited by 100 mmol/l KCl-containing physiological salt solution (KPSS). *P < 0.05 vs. Gla−/0 (by 2-way ANOVA followed by Bonferroni's post hoc test). †P < 0.05 vs. Gla+/0 + respective treatment (by 2-way ANOVA followed by Bonferroni's post hoc test).