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. 2019 Sep 26;33(12):13280–13293. doi: 10.1096/fj.201901002R

Figure 3.

Figure 3

HCD worsened endothelial cell–dependent vasodilation and whisker-evoked CBF in WT mice; EX normalized these responses in both genotypes. A, C) HCD impaired endothelium-dependent dilations to ACh and TRPV4 channel opener GSK1016790A (GSK) in WT mice, but did not worsen the already-altered responses in TGF mice; EX restored these responses to WT control levels (n = 3–5/group). B, D) Smooth muscle cell–mediated dilatory responses to CGRP and Lev were only impaired in TGF and TGF HCD mice and fully normalized by EX. E, F) Group mean traces of CBF responses (n = 4–6/group) to 20-s whisker stimulation (E) and quantification (F) for cohort 2 are shown. HCD impaired CBF increases in WT mice, and EX normalized this response in both WT and TGF groups fed an HCD. *P < 0.05, **P < 0.01, ***P < 0.001: differences between TGF groups; #P < 0.05, ##P < 0.01, ###P < 0.001: differences between WT groups; differences between genotypes are not shown, because of significant interactions between treatment condition and genotype.