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. 2017 Jul 20;113(14):1753–1762. doi: 10.1093/cvr/cvx115

Figure 1.

Figure 1

Mmp2 gene deletion prevented angiotensin (Ang) II-induced endothelial dysfunction and vascular remodelling but not hypertension. Mean 24-h systolic blood pressure (SBP, A) by telemetry and vasodilator responses to acetylcholine (B), vascular stiffness (C), media/lumen (D), and media cross-sectional area (MCSA, E) of small mesenteric arteries using pressurized myography were determined in wild-type (WT) and Mmp2 knockout (Mmp2-/-) mice infused or not with Ang II for 14 days. Media/lumen and MCSA were determined at an intraluminal pressure of 45 mm Hg. Stiffness was determined by comparing values at 140 mm Hg. Values are means ± SEM. Number of samples per group for A: control groups = 3 and Ang II-treated groups = 5. For B: WT = 7, WT + Ang II = 6 and Mmp2-/- and Mmp2-/- + Ang II = 8. For C–E: WT + Ang II = 6 and other groups = 8. Data were analysed using two-way ANOVA for repeated measures in A and B and two-way ANOVA in C–E, with all ANOVA followed by a Student–Newman–Keuls post hoc test. Only the SBP of WT + Ang II and Mmp2-/- +Ang II were statistically analysed in A using respective days 0 as untreated controls. The SBP of WT and Mmp2-/- control groups is presented for reference, and is similar to day 0 of Ang II-treated WT and Mmp2-/- mice. The strain at 140 mm Hg was analysed in C. *P < 0.05 and **P < 0.001 vs. their respective controls and †P < 0.05 and ††P < 0.001 vs. WT + Ang II.