Pulmonary beta-adrenergic receptors and response do not mature precociously in growth-retarded rabbit fetuses.

Growth-retarded infants have a reduced risk of pulmonary morbidity. We used a naturally occurring model of growth retardation in rabbits to test the hypothesis that reduced risk might be related to precocious maturation of the alveolar beta-adrenergic response system in runted neonates. We confirmed that the weights of the fetuses were significantly different, depending on uterine position, as predicted by this model. However, we found no evidence of either increased beta-adrenergic receptor concentration or cyclic adenosine monophosphate generation in the smaller fetuses. These results indicate that reduced fetal size in this model of growth retardation does not result in accelerated maturation of alveolar beta-adrenergic responses in neonates.