Objective: To investigate the effects of fasudil dichloroacetate (FDCA) on hypoxic pulmonary hypertension (HPH) in rats and the potential mechanisms underlying. Methods: SD rats were randomly divided into 4 groups: control (CON) group, CON+FDCA group, chronic hypoxia (CH) group, and CH+FDCA group. The rats in CH and CH+FDCA groups were exposed to chronic hypoxia with (10 ± 0.1) % oxygen for 28 days, and the rats in CON+FDCA and CH+FDCA groups were given FDCA (43.3 mg/kg·d) intragastrically from the 15th day of hypoxia. After 28 days of hypoxia, right ventricular systolic pressure (RVSP), and right ventricular hypertrophy index (RVHI) were assessed. The morphological changes of pulmonary vessels and right ventricle were evaluated by hematoxylin-eosin staining, α-SMA immunohistochemical staining and Masson’s trichome staining. ELISA was used to analyze the contents of interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), the levels of myosin light chain kinase (MLCK), and myosin light chain phosphorylase (MLCP) in lung. The expression of ROCK1 and ROCK2 in rat lung tissue were measured by Western Blot assay. Results: FDCA alleviated hypoxia-induced increments of RVSP and RVHI, as well as cardiomyocytes hypertrophy. In addition, FDCA suppressed hypoxia-induced pulmonary artery wall hypertrophy, pulmonary vessel muscularization and perivascular fibrosis. ELISA showed that FDCA inhibited hypoxia-induced upregulation of IL-1β, IL-6, TNF-α, and restored the expression of MLCK and MLCP in lung. Moreover, FDCA reversed hypoxia-induced upregulation of ROCK1 and ROCK2 in the lung tissue of HPH rats. Conclusion: FDCA alleviates HPH by inhibiting chronic hypoxia-induced pulmonary vascular contraction and remodeling, as well as suppressing inflammation in lung. These results indicate that FDCA could be a potential compound for treating HPH.