AIM：To explore the effects of rosiglitazone, an agonist of peroxisome proliferator-activated receptor γ (PPARγ), on pulmonary vascular endothelial function in the rat model of pulmonary hypertension. METHODS：Forty Sprague-Dawley (SD) rats were divided into 4 groups：normal control group, model group, rosiglitazone group and rosiglitazone plus GW9662 (a specific blocker of PPARγ) group (10 rats in each group). The rat model of pulmonary hypertension was established by subcutaneous injection of monocrotaline at a dose of 60 mg/kg. The rats in normal control group were treated with subcutaneous injection of normal saline. Rosiglitazone (2.0 mg·kg-1·d-1) was given by intragastric administration once a day. GW9662 (0.3 mg·kg-1·d-1) was also given by intragastric administration. Four weeks later, the blood was taken from the abdominal aorta for detecting the levels of endothelin (ET-1) and nitric oxide (NO) by ELISA. The pulmonary artery was isolated, and the vascular activities and the endothelial function were evaluated by wire myograph. Human pulmonary artery endothelial cells (HPAECs) were cultured in DMEM and treated with DMSO, rosiglitazone or rosiglitazone plus GW9662, then NO production in HPAECs was evaluated. RESULTS：Rosiglitazone administration improved the endothelium-dependent relaxation in pulmonary arteries. Rosiglitazone did not affect the endothelium-independent relaxation in pulmonary hypertensive rats. Rosiglitazone also decreased the plasma ET-1 level and increased the NO level in pulmonary hypertensive rats. PPARγ antagonist GW9662 blocked the effects of rosiglitazone mentioned above. Treatment with rosiglitazone significantly increased the NO production in cultured HPAECs, and this effect was also blocked by GW9662. CONCLUSION：Rosiglitazone improves pulmonary vascular endothelial function in the rat model of pulmonary hypertension by activation of PPARγ.