The effects of hypoxia on the potential for the vagus to slow the heart, and on resting heart rate, were compared in anesthetized, vagotomized adult and fetal sheep, and in a chronically catheterized fetus in utero. In adults, the action of the cardiac vagus was potentiated at and below an arterial pO2 in the range 13-27 mm Hg. In contrast, in the fetus and the neonate, vagal action was not potentiated as pO2 fell through this range to 10-12 mm Hg. Below 10-12 mm Hg baseline heart rate fell markedly, and the effect of the cardiac vagus on heart rate was diminished, but its effect on pulse interval was not consistently changed. It is concluded that potentiation of vagal action during hypoxia occurs in adult but not fetal sheep and the bradycardia seen in the fetus during severe hypoxia is probably due to direct myocardial depression.