CGRP suppressed hypertrophy and hyperplasia of VSMCs in vitro and in vivo. VSMCs, stimulated with CGRP (10−7 mol/L) for 60 min or CGRP8‐37 (3 × 10−5 mol/L) for 30 min, were treated with Ang II (10−7 mol/L) for 30 min. In some experiments, NAC (10−2 mol/L) or H2O2 (10−3 mol/L) was applied 30 min before CGRP or Ang II pre‐treatment. A and B, The proliferation of VSMCs was analysed using BrdU assays. C, Systolic blood pressure (SBP) was measured by tail‐cuff plethysmography in three groups: control group (saline‐treated), Ang II (750 µg/kg/d, in saline)‐treated group and Ang II + CGRP (50 nmol/d, in saline)‐treated group (n = 5). D, The medial thickness of the abdominal aortas was assayed in the Ang II‐treated and Ang II + CGRP‐treated groups (n = 5). E, The 8‐OHdG immunohistochemistry of the abdominal aortas in the Ang II‐treated and Ang II + CGRP‐treated groups (n = 5). Bar graphs show mean ± SEM values from three independent experiments. *P < .05, **P < .05 vs Ang Ⅱ. #
P < .05 vs control