Augmented sensitivity to sympathetic mediators occurs in non-infarcted tissues after healing of myocardial infarction. We studied regional beta-adrenergic receptor numbers and adenylate cyclase activity in cat ventricles with healed myocardial infarctions and in the same regions from control hearts. Tissues were obtained from regions remote from and adjacent to the infarct and from the infarct zone itself. Beta-adrenergic receptor numbers were significantly reduced in adjacent and infarcted regions of the healed infarction model. Basal adenylate cyclase activity was increased in tissues remote from and adjacent to the infarct. In remote tissues, total adenylate cyclase activity during maximum isoproterenol stimulation was increased, but the isoproterenol stimulated increment was normal after subtraction of basal activity. In adjacent tissues, total adenylate cyclase activity during isoproterenol stimulation was normal, but the stimulated increment was reduced after subtraction of basal activity. This reduction in activity was reversed when GTP was replaced with Gpp(NH)p. No changes in adenylate cyclase activity, relative to control, were observed in tissues from the infarcted area. These results indicate that chronic changes in the beta-adrenergic receptor/adenylate cyclase system persist after healing of myocardial infarction, and that the nature of the changes are regional depending on proximity to the healed scar.