The study compares the effects of prenatal exposure to terbutaline (a beta-adrenergic agonist) and dexamethansone (a glucocorticoid) on the development of heart rate control mechanisms in the rat. Both drugs produced a persistent reduction in resting heart rate appearing during the 2nd postnatal wk, but by different mechanisms. Terbutaline affected the development of autonomic input from the CNS, characterized by a premature shift from sympathetic to parasympathetic dominance; thus, heart rate differences between terbutaline-exposed animals and controls resolved with acute treatment with a ganglionic blocking agent (chlorisondamine). Dexamethasone did not alter neural input to the myocardium (its actions were not reversed by ganglionic blockade), but instead reduced the intrinsic heart rate; the prenatal glucocorticoid treatment also reduced the sensitivity of the mydocardium to beta-adrenergic stimulation, a factor that could contribute to the alterations in intrinsic rate. (Copyright (c) 1989 International Pediatric Research Foundation, Inc.)