Abstract: AIM To investigate the effect of fasudil on hypoxia-induced remodeling of pulmonary artery and its mechanism. METHODS Hypoxia-induced remodeling model of pulmonary artery were made in BALB/c mice. Mice were divided into three groups: control group, hypoxic group and fasudil group ［15 mg/(kg·day)］, intraperitoneal injection). Hemodynamic measurements and histological studies were performed to detect pulmonary artery remodeling. Expression of canonical transient receptor potential channel 1 (TRPC1) was detected using Western blot and intracellular free calcium concentration (［Ca2+］i) was measured using a fluorescence imaging system. RESULTS Histomorphologic observation showed that chronic hypoxia obviously induced pulmonary artery remodeling, right ventricular wall thickening and higher expression of TRPC1 compared with control group. After treatment with Rho-kinase (ROCK) inhibitor fasudil, hypoxia-induced remodeling in pulmonary artery and right ventricular significantly were inhibited (P<0.05) and the expression of TRPC1 was dramatically decreased (P<0.05). Ca2+ influx in pulmonary artery smooth muscle cells elicited by store depletion using cyclopiazonic acid (CPA) was dramatically augmented in hypoxia group (P<0.05). However, fasudil obviously attenuated this change (P<0.05). CONCLUSION Inhibition of ROCK by fasudil can significantly attenuate hypoxia-induced increase of TRPC1 expression in pulmonary artery and alleviate Ca2+ influx through TRPC1 channel elicited by CPA, which might contribute to hypoxia-induced pulmonary artery remodeling.