Skip to main content
. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: Hypertension. 2017 Oct 16;70(6):1122–1131. doi: 10.1161/HYPERTENSIONAHA.117.09744

Figure 4. Deletion of B1R reduces oxidative stress mediated signaling.

Figure 4

Representative western blots and quantification data for protein expression in the hypothalamic PVN homogenates of wild-type (WT) and B1R gene deletion (B1RKO) mice treated with sham or DOCA-salt for three weeks. Protein expression of Nox2, a catalytic subunit of NADPH Oxidase (A), and inducible nitric oxide synthase (iNOS, B) were significantly increased in hypothalamic PVN indicating increased oxidative stress. However, this increase in oxidative stress was not observed in B1RKO mice. In addition, phosphorylated and total ASK1 (C), phosphorylated and total JNK (D), and phosphorylated and total ERK1/2 (E) protein expression in the PVN indicates activation of ASK1, JNK and ERK1/2 in DOCA-salt hypertension, which was prevented by B1R gene deletion. n=4/group, PVN tissues from 3 mice were pooled for each sample. Data are presented as mean ±SEM. Two-way ANOVA, *P<0.05 vs. WT+Sham, †P<0.05 vs. WT+DOCA.