Involvement of the b-adrenergic system in the cardiac 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 M., GARRIDO VANINA V., PAGLINI-OLIVA PATRICIA A.

PARASITOLOGY

Cambridge Journals

Lugar: Cambridge, UK; Año: 2009 vol. 136 p. 905 - 918

0031-1820

Changes in cardiac b-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; b-receptor density, affinity and function; cardiac cAMP concentration and phosphodiesterase activity, cardiac contractility, and presence of b-receptor autoantibodies. Tulahuen-infected mice presented lower epinephrine and norepinephrine levels; lower b-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 b-receptor interaction. SGO-Z12-infected mice, presented lower norepinephrine levels and epinephrine levels that diminished with the evolution of the infection; lower b-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 b-receptor autoantibodies with strong interaction with the b-receptors. None of the antibodies however, act as b-receptor agonist. Present results demonstrate that this system is seriously compromised in the cardiac chronic stage of T. cruzi infection.