Renewed interest in the use of the embryonic chicken as a model of perinatal cardiovascular regulation has inspired new questions about the control mechanisms that respond to acute perturbations, such as hypoxia. The objectives of this study were to determine the cardiovascular responses, the regulatory mechanisms involved in those cardiovascular responses and whether those mechanisms involved the central nervous system of embryonic chickens. Heart rate and blood pressure were measured in chicken embryos of different incubation ages during exposure to different levels of hypoxia (15, 10 and 5% O₂). At all levels of hypoxia and at all developmental ages, a depression of heart rate and arterial pressure was observed with the exception of day 20 embryos in 15% and 10% O₂. The intensity of the embryonic heart rate and blood pressure responses were directly related to the level of hypoxia used. Muscarinic and -adrenergic receptors stimulation limited the hypoxic hypotension on days 15 to 19 and 15 to 21 respectively as indicated following blockade with atropine and phentolamine. During the final 3 days of incubation the intensity of the hypoxic hypotension was magnified due to a vasodilation caused by ß-adrenergic and muscarinic receptor stimulation. In 19 to 21 day embryos the heart rate response to hypoxia was limited by -adrenergic receptors stimulation as indicated by the accentuated bradycardia following blockade with phentolamine. Further on day 21, atropine limited the hypoxic bradycardia, indicating that muscarinic receptors also play a role in the heart rate response at this stage. In addition, the muscarinic actions on the heart and the adrenergic effects on the vasculature appeared to occur through a hypoxic induced direct release from chromaffin tissue and autonomic nerve terminals. Thus in embryonic chickens the only cardiovascular response to hypoxia that involves the central nervous system was the cholinergic regulation of arterial pressure after day 15 of incubation. Therefore, while embryonic chickens and fetal sheep, the standard model of perinatal cardiovascular physiology, respond to hypoxia with a similar redistribution of cardiac output, the underlying mechanisms differ between these species.