Objective: To investigate the effect of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on pulmonary vascular remodeling in monocrotaline-induced mice model of pulmonary artery hypertension. Methods: CD1 male mice were randomly divided into control group, monocrotaline group, and monocrotaline+nicorandil group(n=6 for each group). The latter 2 groups were subcutaneously injected with 400 mg/kg monocrotaline weekly for 8 weeks to induce pulmonary artery hypertension model. The mice in the monocrotaline+nicorandil group were treated with 10.5 mg/kg nicorandil daily by intragastric administration. After 8 weeks, the right ventricular systolic pressure was evaluated by right ventricular puncture through the diaphragm; the index of right ventricular hypertrophy was calculated; the morphologic changes of right ventricle cardialmyocytes were detected by HE staining; the thickness of pulmonary arterial media wall was measured by elastin staining; α-smooth muscle actin (α-SMA) immunohistochemitry was used to assay pulmonary arterioles muscularization. Results: Daily treated with nicorandil (10.5 mg/kg) for 8 weeks significantly decreased RVSP (P<0.01), attenuated the index of right ventricular hypertrophy (P<0.05), alleviated the thickness of pulmonary arterial media wall (P<0.01), declined the ratio of fully-muscularized pulmonary arterioles (P<0.01), and prevented the injury of right ventricle cardialmyocytes. Conclusion: Nicorandil could relieve monocrotaline-induced pulmonary artery hypertension by inhibiting pulmonary vascular remodeling. It could be a potential drug for preventing and treating pulmonary artery hypertension.