In situ hybridization of angiotensin receptor mRNA and ligand-binding assay showed that main subtype of angiotensin receptor in the lung was type 1(AT1) in pulmonary vessel, whereas type 2(AT2) was not detectable. AT1 induces the pulmonary artery contraction through inositol phosphate-protein kinase C pathway, therefore the non-peptide AT1 antagonist was applied to animal model of pulmonary hypertension (PH). AT1 antagonist improved pulmonary arterial remodeling and right ventricular hypertrophy in rat hypoxia-induced PH but not in rat monocrotaline-induced PH. Less effectiveness of AT1 antagonist for PH might be no AT2 stimualtion under increased angiotensin II level in blood and lung tissue response to AT1 antagonist treatment.