Imbalances of ß-adrenoceptor (ß-AR) and muscarinic acetylcholine receptor (mAChR) input are thought to underlie perinatal cardiovascular abnormalities in conditions such as Sudden Infant Death Syndrome. Administration of isoproterenol, a ß₁/ß₂-AR agonist, to neonatal rats on postnatal (PN) days 2-5 caused downregulation of m2-AChRs and a corresponding decrement in their control of adenylyl cyclase activity. Terbutaline, a ß₂-selective agonist that crosses the placenta and the blood-brain-barrier, was also effective when given either on PN2-5 or during gestational (GD17-20). Terbutaline failed to downregulate brain m2-AChRs, even though it downregulated ß-ARs; ß-ARs and m2-AChRs are located on different cell populations in the brain, but on the same cells in the heart. Destruction of catecholaminergic neurons with neonatal 6-hydroxydopamine upregulated cardiac, but not brain m2-AChRs. These results suggest that perinatal ß-AR stimulation shifts cardiac receptor production away from the generation of m2-AChRs, so that the development of sympathetic innervation acts as a negative modulator of cholinergic function. Accordingly, tocolytic therapy with ß-AR agonists may compromise the perinatal balance of adrenergic and cholinergic inputs.