AAC-induced LV pressure overload leads to concentric hypertrophy. (A) Parasternal short axis (PSAX) projection with M-mode was used to quantify left ventricle structure and function. Scale bars, 5 mm (upper panels), horizontal bars represent 100 ms. (B) LViDd, LVIDs, LVEF in LV from Sham-WT (n = 7), Sham-Kcnk3Δ94Ex1/Δ94Ex1 (n = 7–8), AAC-WT (n = 8), and AAC-Kcnk3Δ94Ex1/Δ94Ex1 rats (n = 9). (C) LVWT, RWT in LV from Sham-WT (n = 7), Sham-Kcnk3Δ94Ex1/Δ94Ex1 (n = 8), AAC-WT (n = 8), and AAC-Kcnk3Δ94Ex1/Δ94Ex1 rats (n = 9). (D) Immunofluorescence images of LV sections stained with FITC-conjugated wheat germ agglutinin (WGA, 50 μg/mL, green) and 4′,6-diamidino-2-phenylindole (DAPI, blue). Scale bar, 50 μm. (E) Quantification of cardiomyocytes cross section area (CSA, five different rats for each group). (F) LV/TL in Sham-WT (n = 5), Sham-Kcnk3Δ94Ex1/Δ94Ex1 (n = 10), AAC-WT (n = 11), and AAC-Kcnk3Δ94Ex1/Δ94Ex1 rats (n = 15). (G) Schematic representation of concentric LV hypertrophy. (H) Relative mRNA expression (2−ΔΔCt) of kcnk3 in LV, RV, lung from Sham-WT (n = 5–6), and AAC-WT rats (n = 5–6). Experiments were normalized to 18S mRNA and statistical analysis performed using ΔCt values. Data are represented as scatter dot plots, with mean ± SEM. Experiments presented in panels A–D and F–H were analysed using two-way ANOVA followed by Sidak’s post hoc test, and experiments presented in panel E were analysed using one-way ANOVA followed by Dunn’s post hoc test after Kruskal–Wallis test, **P < 0.01, ****P < 0.0001. LVEF, LVWT, cardiomyocyte CSA, and LV/TL were not normally distributed and were log-transformed prior to statistical analysis.
