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

doi:10.1042/cs103s064s

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 journal › Article › peer-review

13 Scopus citations

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 ET_A 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 ET_A 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 language	English (US)
Pages (from-to)	64S-67S
Journal	Clinical science
Volume	103
Issue number	SUPPL. 48
DOIs	https://doi.org/10.1042/cs103s064s
State	Published - Aug 2002
Externally published	Yes

Keywords

Bradykinin
Heart failure
Langerdorff
Nitric oxide

ASJC Scopus subject areas

General Medicine

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10.1042/cs103s064s

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title = "Role of endothelin during experimental Trypanosoma cruzi infection in rats",

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.",

keywords = "Bradykinin, Heart failure, Langerdorff, Nitric oxide",

author = "Camargos, {Elizabeth R.S.} and Machado, {Concei{\c c}{\~a}o R.S.} and Teixeira, {Antonio L.} and Rocha, {Lamara L.V.} and Ferreira, {Anderson J.} and Almeida, {Alvair P.} and Matthias Barton and Teixeira, {Mauro Martins}",

year = "2002",

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doi = "10.1042/cs103s064s",

language = "English (US)",

volume = "103",

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AU - Camargos, Elizabeth R.S.

AU - Machado, Conceição R.S.

AU - Teixeira, Antonio L.

AU - Rocha, Lamara L.V.

AU - Ferreira, Anderson J.

AU - Almeida, Alvair P.

AU - Barton, Matthias

AU - Teixeira, Mauro Martins

PY - 2002/8

Y1 - 2002/8

N2 - 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.

AB - 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.

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KW - Heart failure

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KW - Nitric oxide

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Role of endothelin during experimental Trypanosoma cruzi infection in rats

Abstract

Keywords

ASJC Scopus subject areas

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