The mechanism of release of
catecholamines from the adrenal medulla of neonatal rats was examined, together with the role of these
amines in the ability of the organism to withstand acute O2 deprivation. Splanchnic innervation of the rat adrenal is non-functional until the end of the first postnatal week. Nevertheless,
hypoxia caused depletion of adrenal
catecholamines in 1-day-old rats as well as in 8-day-old animals. Pre-treatment with
cholinergic receptor blocking agents did not prevent the
catecholamine response at 1 day but did in older animals; these results indicate that the depletion mechanism is not neurogenic in 1-day-old animals but is neurogenic in 8-day-old animals. The proportions of
noradrenaline and
adrenaline released by hypoxic stress also differed at the two ages, with preferential release of
adrenaline by the neurogenic mechanism but not by the non-neurogenic one. The ontogenetic replacement of non-neurogenic adrenomedullary responses by the neurogenic mechanism was directly related to the onset of splanchnic nerve function. Treatments which accelerated the development of neuronal connexions (neonatal
hyperthyroidism, maternal stress) caused premature loss of the non-neurogenic response. Prior to the development of sympathetic nerve function, adrenal
catecholamines plays a predominant role in enabling the neonate to survive
hypoxia. Interference with the release of adrenal
amines invariably increased mortality during
hypoxia. In contrast, interference with sympathetic neural release of
catecholamines did not affect the ability of 1-day-old rats to withstand
hypoxia, indicating that survival during low PO2 conditions is not dependent on the sympathetic innervation at that stage of development. After functional development of the sympathetic nerves and disappearance of non-neurogenic adrenomedullary responses, the neonatal rats became partially dependent upon
catecholamines derived from sympathetic terminals; administration of
bretylium at 8 days significantly compromised survival during
hypoxia. Interference with
adrenergic receptor function also interfered with the ability of neonatal rats to withstand low PO2. At 1 day of age, either
phenoxybenzamine or
ICI-118551, but not
atenolol, shortened the survival time during
hypoxia. At 8 days, only
phenoxybenzamine did so.(ABSTRACT TRUNCATED AT 400 WORDS)