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. Author manuscript; available in PMC: 2013 Sep 1.
Published in final edited form as: J Neurochem. 2012 Aug 3;122(6):1211–1218. doi: 10.1111/j.1471-4159.2012.07872.x

Figure 4.

Figure 4

Figure 4

(A) Superoxide anion production in the cerebral microvessels of hph-1-/- and hph-1+/- mice. Basal superoxide production between wild-type male and female mice was not statistically significant. Superoxide anion production remained significantly increased in male and female cerebral microvessels in both hph-1-/- and hph-1+/- groups (* P<0.05, in comparison to their wild-type controls, n=8). Treatment with L-NAME (30 μmol/l) significantly reduced the superoxide anion production in cerebral microvessels of both hph-1-/- and hph-1+/- mice (# P<0.05 in L-NAME treated group as compared to corresponding sex-matched vehicle (Krebs-HEPES buffer) treatment, n=8). (B) Superoxide anion production in microvessels of female wild-type, hph-1-/- and hph-1+/-mice injected with BH4 (100 μmol/kg, 3hours). Treatment with BH4 abolished the increase in superoxide anion production observed in cerebral microvessels of hph-1-/-and hph-1+/- mice. Treatment with L-NAME (30 μmol/l) did not have any further effect on the superoxide anion production (P=ns, n=4).