Figure 3.

Physiology underlying the fetal cardiovascular defense to acute hypoxia. Activation of a carotid chemoreflex by hypoxic blood triggers a fall in heart rate and vasoconstriction in the peripheral circulation in the fetus. The fall in heart rate is vagally mediated and the peripheral vasoconstriction is initiated by activation of the sympathetic nerves. Vasoconstrictor hormones, such as catecholamines and vasopressin are then released into the fetal circulation to maintain the neurally-triggered vasoconstriction. The neuroendocrine vasoconstriction is then supplemented by a vascular oxidant tone, which is promoted by an increase in the ratio of free radicals, such as the superoxide anion (O2^•-) relative to nitric oxide (NO), both of which are increased in the fetus during periods of oxygen deprivation. The magnitude of the peripheral vasoconstrictor response to acute hypoxia in the late-gestation fetus therefore depends on the partial contributions of chemoreflex, endocrine, and local vascular redox responses. Redrawn from Giussani¹¹ with permission. Copyright ©2016, The Physiological Society.