AIM: To investigate the role of nitric oxide (NO)in the development of chronically hypoxic pulmonary artery hypertension (PAH) and the hemodynamic effects of inhaled NO on pulmonary circulation. METHODS: 67 male adult SD rats were randomly divided into 7 groups: (1) control ( n= 9);(2) chronically intermitent hypoxia (CIH, 6 h/d, 7 d/w) 1 week( n= 7); (3) CIH 2 weeks ( n= 11); (4) CIH 3 weeks ( n= 11); (5) CIH 1 week+L-NAME (NO synthase inhibitor, 30 mg/kg, by gavage, n= 10); (6)CIH 3 weeks+L-Arg (NO precursor, 10 mg/kg, by gavage, n= 9); (7) CIH 3 weeks+inhaled NO (0.0004% for 20 min, n= 10) to determine the mean pulmonary artery pressure (MPAP), weigh the right ventricle (R) and ventricular segment plus left ventricle (S+L), and calculate R/(S+L) (g/g) and R/Wt (Wt: body weight, g/kg). RESULTS: 1.MPAP increased compared with control [(3 2?0.3 ) kPa vs (1.8?0.3) kPa, P