YAP upregulation by Ang II. An HVR rat model was established by continuous Ang II infusion for 2 weeks. YAP was knockdown by adventitial application of the Ad‐YAP‐shRNA. Values were presented as the mean ± SEM. A, Temporal trend of SBP and heart rate which were measured using a caudal artery tail‐cuff system on days 0, 3, 7, and 14 after treatment. B and C, Ang II regulated YAP and LATS1 expression and phosphorylation in the RCCAs. Densitometric quantification and representative western blots of total protein lysates for YAP and LATS1 were shown. Data were normalized to the housekeeping proteins GAPDH. D, Ang II regulated the gene expression of Yap1 and Last1 were analysed using quantitative real‐time polymerase chain reaction. Data were expressed relative to the control (set to 1) after normalization to GAPDH (served as an internal control). E, Immunohistochemical staining of YAP in RCCAs. F, Quantitative analysis of the relative MOD (related to the control group) shown in (E). *P < 0.05 compared with the control group, **P < 0.01 compared with the control group; #P < 0.05 compared with the Ang II + Ad‐GFP group, ##P < 0.01 compared with the Ang II + Ad‐GFP group. HVR, hypertensive vascular remodelling; RCCA, right common carotid artery; MOD, mean optical density; SBP, systolic blood pressure; LATS1, large tumour suppressor kinase 1; GAPDH, glyceraldehyde phosphate dehydrogenase (n = 5)