To investigate whether the acute hypoxia can be a stimulus for atrial natriuretic peptide (ANP) secretion, plasma levels of ANP were determined under three different hypoxic conditions in six normal subjects. During 15% O2 breathing for 10 min, no significant change in plasma ANP level was observed. Severe hypoxia induced by 10% O2 breathing increased the mean pulmonary arterial pressure (Ppa) by 11.6 mm Hg within 10 min (P less than 0.01), accompanying a slight but significant rise in plasma ANP level of pulmonary artery (PA) from 24.3 +/- 5.3 to 28.2 +/- 4.6 pg/ml (P less than 0.05). There was a tendency for the ANP level of PA to rise under hypoxic hypobaria at 515 Torr for 10 min, followed by a decrease of that level during 100% O2 breathing under hypobaric condition. These changes, however, still remained in the normal range. No significant changes were observed both in right atrial pressure and in pulmonary capillary wedge pressure under any of the three hypoxic conditions. From these results we conclude that ANP can be released in response to the elevation of Ppa caused by acute hypoxia in normal subjects, but the changes in plasma ANP level may be too small to play a significant physiological role in hemodynamic responses to acute hypoxia.