Fetal catecholamines.

Experimental data from fetal human and animal research suggest that the fetal sympathoadrenal system, composed of the adrenal medulla, sympathetic neurons, and extra-adrenal chromaffin tissue functions from early fetal life to maintain fetal homeostasis. The extra-adrenal chromaffin tissue undergoes maturation at 9 to 11 weeks of gestation, whereas the adrenal medulla and sympathetic nervous system mature later in fetal life. The fetal catecholamine response to hypoxia, mediated predominantly by norepinephrine, is an important component of the fetal cardiovascular response to hypoxia, i.e., through alpha-receptor stimulation, fetal cardiac output redistribution occurs. Fetal catecholamine secretion in response to substrate availability, through alpha- and beta-receptor stimulation, provide a mechanism by which the fetus can utilize its own substrate stores. Pulmonary beta-receptor stimulation by catecholamines has been demonstrated to increase lecithin synthesis, increase surfactant secretion, and decrease lung fluid production near term. beta-Receptor stimulation has also been demonstrated to have trophic effects on the development of thermogenic brown adipose tissue. Although the exact stimulus for the initiation of parturition in the primate is unknown, fetal catecholamines, through direct myometrial alpha-adrenergic or dopaminergic receptor stimulation and/or through the stimulation of prostaglandin production, have the potential of facilitating the onset of parturition.