BACKGROUND: This study was performed with NW-nitro-L-arginine methyl ester ((L)-NAME), an inhibitor of EDRF production, and glibenclamide, which closes ATP dependent K+ channels, to determine their effects on hypoxic pulmonary vasoconstriction in isolated perfused rat lungs ventilated with normoxia (21% O2, 5% CO2, balanced N2) and hypoxia (5% O2, 5% CO2, balanced N2). METHODS: Thirty male Sprague-Dawley rats (250 - 350 g) were divided into the control group (n = 10), glibenclamide group (n = 10), and (L)-NAME group (n = 10). In the control group, after the lungs were isolated and stabilized, they were exposed to angiotensin II and 3 consecutive hypoxias. In glibenclamide group, they were exposed to angiotensin II and 3 consecutive hypoxias, and exposed to 3 more hypoxias after injection of glibenclamide 10 uM. In the (L)-NAME group, they were exposed to angiotensin II and 3 consecutive hypoxias, and exposed to 3 more hypoxias after injection of (L)-NAME 100 uM. RESULTS: Hypoxic pulmonary vasoconstriction (deltaPpa) after the (L)-NAME 100nM injection was 12.5 +/- 1.1 mmHg, and it was significantly greater than that of the control group 4.2 +/- 1.1 mmHg (P < 0.05). Hypoxic pulmonary vasoconstriction (deltaPpa) after glibenclamide 10nM injection was 5.3 +/- 1.1 mmHg, and there was no difference with the control group, 4.2 +/- 1.1 mmHg. CONCLUSIONS: We concluded that (L)-NAME, an inhibitor of EDRF production, significantly increased hypoxic pulmonary vasoconstriction, but glibenclamide, which closes ATP dependent K+ channels, did not affect hypoxic pulmonary vasoconstriction in this model.