Role of endothelin during experimental Trypanosoma cruzi infection in rats-Reference-Cited by-同舟云学术

Role of endothelin during experimental Trypanosoma cruzi infection in rats

Published:2002-09-01 Issue:s2002 Volume:103 Page:64S-67S
ISSN:0143-5221
Container-title:Clinical Science
language:en
Short-container-title:

Author:

CAMARGOS Elizabeth R.S.¹,MACHADO Conceição R.S.¹,TEIXEIRA Antonio L.¹,ROCHA Lamara L.V.¹,FERREIRA Anderson J.²,ALMEIDA Alvair P.²,BARTON Matthias³,TEIXEIRA Mauro M.⁴

Affiliation:

1. Department of Morphology, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Avenida Antônio Carlos 6627, Belo Horizonte, Minas Gerais, Brazil

2. Department of Physiology and Biophysics, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Avenida Antônio Carlos 6627, Belo Horizonte, Minas Gerais, Brazil

3. Department of Medicine and Medical Policlinic, University Hospital Zurich, Zurich, Switzerland

4. Biochemistry and Immunology, Instituto de Ciências Biológicas, Federal University of Minas Gerais, Avenida Antônio Carlos 6627, Belo Horizonte, Minas Gerais, Brazil

Abstract

Chagas' disease is caused by the intracellular protozoan Trypanosoma cruzi. Here we have investigated the role of endothelin-1 in T. cruzi acute infection in rats, using the orally active ETA receptor antagonist BSF-461314. Treatment with BSF-461314 markedly increased parasitaemia, but animals managed to control the infection by day 15. Histopathological analysis of heart tissue at the end of the acute phase showed greater numbers of parasite nests in BSF-461314-treated animals. The perfusion of isolated rat hearts from infected animals with bradykinin failed to induce an increase, and actually reduced, coronary blood flow. Pretreatment with BSF-461314 prevented changes in coronary flow induced by T. cruzi infection. Together these results demonstrate that endothelin-1, through ETA receptor activation, contributes to the protective immune response against acute T. cruzi infection. Moreover, these data suggest that endothelin-1 is a mediator of impaired endothelium-dependent vasomotion in the coronary microcirculation associated with acute T. cruzi infection.

Publisher

Portland Press Ltd.

Subject

General Medicine

Link

https://portlandpress.com/clinsci/article-pdf/103/s2002/64S/440180/cs103s064s.pdf

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