Hypoxaemia in fetal sheep causes a decrease in vascular resistance of the heart, brain and adrenal gland which results in increased blood flow to these organs. Placental blood flow is maintained. To investigate whether increased beta-adrenergic activity during hypoxaemia is involved in these changes, the effects of propranolol on organ blood flows (using the microsphere method) and other cardiovascular variables were studied during fetal hypoxaemia (50% reduction of fetal haemoglobin saturation) in 5 chronically catheterized fetal sheep at 126 to 130 days of gestation. Beta-blockade during hypoxaemia caused a fetal bradycardia and a 30% drop in cardiac output. Placental and myocardial blood flows fell by 39% and 37% respectively. Total peripheral resistance increased by 35% mainly due to increased fetal placental vascular resistance. Heart and lung vascular resistances increased following propranolol. In 3 similarly catheterized animals, propranolol administered in the absence of hypoxaemia led to a 9% drop in cardiac output and placental blood flow but no redistribution of blood flow to fetal organs. It is concluded that the increased beta-adrenergic activity associated with fetal hypoxaemia limits the negative chronotropic effects of concomitantly increased vagal activity, maintains placental blood flow through its inotropic and chronotropic activity as well as by maintenance of placental vasodilatation and may be one of several factors which increase myocardial blood flow during hypoxaemia.