It has been reported that hyperventilation (HV) increases the release of vasodilative prostaglandins (PGs) from animal lungs. However, it has not yet been clarified whether or not the results obtained from animal experiments are applicable to humans. To confirm this point, we performed this study. Healthy male volunteers, aged 22-28 years, were divided into two groups. Group I (n = 11) breathed room air and showed respiratory alkalosis. Group II (n = 11) breathed room air containing 5% CO2 and maintained normal arterial blood pH. Each subject hyperventilated voluntarily and vigorously for 10 min. The mean values of respiratory rates, tidal volumes and minute volumes during HV were 42.1 +/- 6.2 breaths/min, 1390 +/- 280 ml and 58.5 +/- 15.2 l/min, respectively. Arterial and venous blood samples were drawn simultaneously before and after HV from brachial artery and medial cubital vein, respectively. Plasma 6-keto PGF1 alpha, a metabolite of PGI2, and PGE2 were measured by radioimmunoassay (RIA). After HV, concentrations of 6-keto PG F1 alpha and PGE2 in both arterial and venous blood were increased significantly. There were no significant differences in the levels of 6-keto PGF1 alpha and PGE2 between two groups, nor between arterial and venous blood either before or after HV. We concluded that voluntary HV stimulates the release of PGI2 and PGE2 from lung in humans and respiratory alkalosis has no significant effect on the release of PGs.