Role of endothelin during experimental Trypanosoma cruzi infection in rats

Elizabeth R.S. Camargos, Conceição R.S. Machado, Antonio L. Teixeira, Lamara L.V. Rocha, Anderson J. Ferreira, Alvair P. Almeida, Matthias Barton, Mauro Martins Teixeira

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)64S-67S
JournalClinical science
Issue numberSUPPL. 48
StatePublished - Aug 2002
Externally publishedYes


  • Bradykinin
  • Heart failure
  • Langerdorff
  • Nitric oxide

ASJC Scopus subject areas

  • General Medicine


Dive into the research topics of 'Role of endothelin during experimental Trypanosoma cruzi infection in rats'. Together they form a unique fingerprint.

Cite this