Involvement of the beta adrenergic system in the cardiac chronic form of the experimental Trypanosoma cruzi infection.

LO PRESTI M. SILVINA; RIVAROLA H. WALTER; FERNÁNDEZ ALICIA R; ENDERS JULIO E; LEVIN GLORIA; FRETES RICARDO; CERBAN FABIO; GARRIDO VANINA; PAGLINI PATRICIA

PARASITOLOGY

Cambridge University Press

Lugar: England; Año: 2009 vol. 136 p. 905 - 918

0031-1820

Summary Changes in cardiac â-adrenergic system had been described in early stages of Trypanosoma cruzi infection. Here, we studied an early (135 days post infection – d.p.i.) and a late stage (365 d.p.i.) of the cardiac chronic form of the experimental infection (Tulahuen or SGO-Z12 strains), determining: plasmatic epinephrine and norepinephrine levels; β-receptor density, affinity and function; cardiac cAMP concentration and phosphodiesterase activity, cardiac contractility, and presence of β-receptor autoantibodies. Tulahuen-infected mice presented lower epinephrine and norepinephrine levels; lower β-receptor affinity and density; diminished norepinephrine response; 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. Tulahuen strain induced autoantibodies with weak β-receptor interaction. SGO-Z12-infected mice, presented lower norepinephrine levels and epinephrine levels that diminished with the evolution of the infection; lower β-receptor affinity and an increased density; unchanged epinephrine and norepinephrine response in the early and a diminished one in the late stage; higher cAMP levels and unchanged basal contractility. SGO-Z12 isolate induced β-receptor autoantibodies with strong interaction with the â-receptors. None of the antibodies however, act as β-receptor agonist. Present results demonstrate that this system is seriously compromised in the cardiac chronic stage of T. cruzi infection. .