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Involvement of the β-adrenergic system in the cardiac chronic form of experimental Trypanosoma cruzi infection

Published online by Cambridge University Press:  15 June 2009

M. S. LO PRESTI*
Affiliation:
Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Santa Rosa 1085, PC5000, Córdoba, Argentina Instituto de Investigación en Ciencias de la Salud Humana, Universidad Nacional de La Rioja. Argentina
H. W. RIVAROLA
Affiliation:
Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Santa Rosa 1085, PC5000, Córdoba, Argentina Instituto de Investigación en Ciencias de la Salud Humana, Universidad Nacional de La Rioja. Argentina
A. R. FERNÁNDEZ
Affiliation:
Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Santa Rosa 1085, PC5000, Córdoba, Argentina
J. E. ENDERS
Affiliation:
Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Santa Rosa 1085, PC5000, Córdoba, Argentina
G. LEVIN
Affiliation:
Centro de Investigaciones Endocrinológicas – CONICET, Hospital de Niños Ricardo Gutiérrez, Gallo 1360, Ciudad Autónoma de Buenos Aires, CP1425, Argentina
R. FRETES
Affiliation:
Cátedra de Biología Celular, Histología y Embriología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, 5016Córdoba, Argentina
F. M. CERBAN
Affiliation:
CIBICI-CONICET, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina
V. V. GARRIDO
Affiliation:
CIBICI-CONICET, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina
P. PAGLINI-OLIVA
Affiliation:
Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Santa Rosa 1085, PC5000, Córdoba, Argentina Instituto de Investigación en Ciencias de la Salud Humana, Universidad Nacional de La Rioja. Argentina
*
*Corresponding author: Pio Collivadino 4126, Cerro Chico, 5009Córdoba, Argentina. Tel/Fax: +54 351 4332020. E-mail: [email protected]

Summary

Changes in the cardiac β-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, β-receptor density, affinity and function, cardiac cAMP concentration and phosphodiesterase activity, cardiac contractility, and the presence of β-receptor autoantibodies. Tulahuen-infected mice presented lower epinephrine and norepinephrine levels; lower β-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 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 response in the late stage; higher cAMP levels and unchanged basal contractility. The SGO-Z12 isolate induced β-receptor autoantibodies with strong interaction with the β-receptors. None of the antibodies, however, acted a as β-receptor agonist. The present results demonstrate that this system is seriously compromised in the cardiac chronic stage of T. cruzi infection.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2009

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