Extended Data Fig. 3: Ex vivo vascular reactivity (VR) of middle cerebral and mesenteric arteries from 16p11.2df/+ and WT mice at P50.
From: Vascular contributions to 16p11.2 deletion autism syndrome modeled in mice
a, Schematic representation of cellular and molecular VR mechanisms. b, Upper panels, Wire myography of mesenteric arteries ex vivo confirming 16p11.2 deletion-induced endothelial dysfunction. Females and males display a similar endothelial-dependent deficit, but normal VSMC response. Lower panels, pD2 values obtained from the dose-response curves from male and female mice. c, pD2 values obtained from dose-response curves of male and female middle cerebral arteries (see Fig. 2). ACh, acetylcholine; L-NNA, NG-Nitro-L-arginine; PE, phenylephrine; SNP, sodium nitroprusside; VSMC, vascular smooth muscle cell; WT, Wild-Type. Data are mean ± s.e.m. in b (upper panel), or whisker boxes (min to max, center line indicating median) in b (lower panel) and c (n = 5-7 animals per sex group). *P < 0.05 (2-way repeated measure ANOVA and Tukey’s post-hoc test in b).
