To determine the importance of beta-adrenergic activity during hypoxia in the fetus, 13 studies were carried out on seven chronically instrumented sheep at nine tenths of gestation. Hypoxia was induced by having the mother breathe gas mixtures that resulted in a reduction of maternal arterial oxygen tension to 32 mm Hg. Hypoxia resulted in a decrease in fetal heart rate (165 +/- 17 to 140 +/- 28 bpm) and fetal oxygen consumption (5.9 +/- 1.3 to 3.0 +/- 1.5 ml/min/kg) and increases in fetal arterial and umbilical venous pressures. There was no change in umbilical blood flow (209 +/- 58 ml/min/kg). Propranolol, 1.1 ml/kg, was rapidly infused into a fetal vein to achieve complete beta-adrenergic blockade. Umbilical vascular resistance increased significantly, fetal heart rate decreased to 112 +/- 22 bpm, and umbilical blood flow decreased to 165 +/- 73 ml/min/kg. There was no further decrease in fetal oxygen consumption. These decreases are approximately twice those seen after propranolol without hypoxia. These findings suggest that during hypoxia there is an increase in beta-adrenergic activity, which tends to maintain fetal heart rate and umbilical blood flow. This activity counteracts the increase in vagal activity with hypoxia, which decreases heart rate.