The levels and turnovers of NE, DA and 5HT were determined in whole brain, brain stem, cervical and thoracic spinal cord and carotid bodies (CB) of rats exposed to from 1 h to 7 days of hypobaric hypoxia (PB = 450 torr). Monoamine levels decreased only transiently upon acute exposure to hypoxia. Monoamine turnover in the CNS was estimated from the average of (a) monoamine buildup following inhibition of catabolism, and (b) monoamine breakdown following inhibition of synthesis. Hypoxic effects on CNS monoamine turnover showed that: (a) NE was not affected; (b) DA was not affected in acute hypoxia, but was reduced to about 40% of normoxia control after 1-7 days hypoxia; (c) 5HT fell 50-60% during acute hypoxia but returned to and was maintained at control over 1-7 days of hypoxia; (d) acute restoration of normoxia following acute hypoxia restored 5HT and DA to control or above and in the acclimatized animal acute normoxia increased DA and 5HT turnover to about 1.4 and 1.8 X control. In the CB, DA levels gradually increased to 4 X control after 7 days of hypoxia and further increased to 6 X control upon acute restoration of normoxia. Changes in the metabolism of both central 5HT and CB DA may be related to the mechanisms mediating ventilatory acclimatization to chronic hypoxia.