Figure 5.

Hypercholesterolemia‐induced reduction in nitric oxide (NO) detection following intraluminal flow is inwardly rectifying K⁺ (Kir) dependent in mouse mesenteric arteries. A, Representative images (×40 magnification) of mesenteric arteries exposed to flow (Δ60 cm H₂O for 30 minutes; right column) or arteries incubated under no flow conditions for the same duration (left column). An increase in NO detection by the NO‐specific dye, diaminorhodamine‐4M, is only present in the wild‐type (WT; top row) artery, while no noticeable increase is observed in apolipoprotein E–deficient (Apoe ^−/−; middle row) or Kir2.1 ^+/− /Apoe ^−/− (bottom row) arteries. B, Group data were generated by taking the fold increase from arteries that received flow to those arteries that did not. Arteries analyzed in this way were always from the same mouse (4 pairs of arteries from 4 mice for all groups). Significant differences exist in NO detection after flow when comparing either Apoe ^−/− model with WT. Bonferroni post hoc analysis followed 1‐way ANOVA. *P<0.05 vs WT. C, Representative blot showing phosphorylated Akt (Ser473) in WT and Apoe ^−/− whole mesenteric arcades. D, Group data revealing a significant decrease in Apoe ^−/− pAkt after normalizing to respective total Akt bands. E, Representative blots showing phosphorylated endothelium NO synthase (eNOS) (Ser1177) in WT and Apoe ^−/− whole mesenteric arcades. F, Group data revealing a significant decrease in Apoe ^−/− peNOS after normalizing to respective total eNOS bands.