Involvement of the [beta]-adrenergic system in the cardiac chronic form of experimental Trypanosoma cruzi infection

SUMMARY Changes in the cardiac [beta]-adrenergic system in early stages of Trypanosoma cruzi infection have been described. Here, we studied an early (135 days post-infection-p.i.) and a late stage (365 days p.i.) of the cardiac chronic form of the experimental infection (Tulahuen or SGO-Z12 strains), determining plasma epinephrine and norepinephrine levels, [beta]-receptor density, affinity and function, cardiac cAMP concentration and phosphodiesterase activity, cardiac contractility, and the presence of [beta]-receptor autoantibodies. Tulahuen-infected mice presented lower epinephrine and norepinephrine levels; lower [beta]-receptor affinity and density; a diminished norepinephrine response and higher cAMP levels in the early stage, and a basal contractility similar to non-infected controls in the early and augmented in the late stage. The Tulahuen strain induced autoantibodies with weak [beta]-receptor interaction. SGO-Z12-infected mice presented lower norepinephrine levels and epinephrine levels that diminished with the evolution of the infection; lower [beta]-receptor affinity and an increased density; unchanged epinephrine and norepinephrine response in the early and a diminished response in the late stage; higher cAMP levels and unchanged basal contractility. The SGO-Z12 isolate induced [beta]-receptor autoantibodies with strong interaction with the [beta]-receptors. None of the antibodies, however, acted a as [beta]-receptor agonist. The present results demonstrate that this system is seriously compromised in the cardiac chronic stage of T. cruzi infection. [PUBLICATION ABSTRACT]