FIGURE 2.
CGRP inhibited oxidative stress via receptors/ cAMP‐PKA‐dependent pathway. VSMCs, stimulated with CGRP (10−6‐10−8 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, dibutyl‐cAMP (10−3 mol/L) was applied for 60 min and H‐89 was applied 30 min before CGRP pre‐treatment. A, Quantitative real‐time PCR analysis of the mRNA levels of CRLR, RAMP1 and RCP in VSMCs. B, Western blot analyses of protein levels of CRLR, RAMP1 and RCP in VSMCs. C, Quantification of intracellular ROS levels in VSMCs after pre‐treatment with dibutyl‐cAMP or H‐89. D, Quantitative real‐time PCR analysis of mRNA levels of p47phox in VSMCs. E, Western blot analysis of membrane and cytoplasmic fractions of p47phox in VSMCs. Bar graphs show mean ± SEM values from three independent experiments. *P < .05, **P < .01 and ***P < .001 vs Ang II. # P < .05 vs control. + P < .05 vs CGRP + Ang II