This study compares the effects of prenatal exposure to terbutaline (a beta-adrenergic agonist) and dexamethasone (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 myocardium to beta-adrenergic stimulation, a factor that could contribute to the alterations in intrinsic rate. These results suggest the potential need for studies of the functional cardiovascular consequences of fetal or neonatal therapeutic interventions with glucocorticoids or adrenergic agents.