We examined the possible role of altered humoral immunity in Chagas' disease by analyzing the effect of sera on the binding of radioligand to beta-adrenoceptors during the course of human Trypanosoma cruzi infection. We described two circulating IgG which bind with myocardial beta 1- and spleen cell beta 2-adrenoceptor. Both chagasic IgG against beta 1- and beta 2-adrenoceptors increased intracellular levels of cAMP, which could be blocked by specific beta 1- and beta 2-adrenoceptor antagonists. The IgG against the beta 1-adrenoceptor inhibited the action of norepinephrine on the contractility of atria. We also found differences in the distribution of beta 1- and beta 2-adrenoceptor antibodies in the course of infection. The anti-beta 2-adrenoceptor IgG appears during the acute stage, peaks on the group with less than 10 years of infection, and then decreases. The prevalence of anti-beta 1-adrenergic antibody is low in the acute stage, but it increases over time since infection, being higher in the group with more than 15 years of infection. The probable pathogenic role of both beta 1- and beta 2-adrenergic chagasic antibodies is discussed.