Trypanosoma cruzi induces endothelin release from endothelial cells

Murray Wittner, George J. Christ, Huan Huang, Louis M. Weiss, Victor B. Hatcher, Stephen A. Morris, George A. Orr, Joan W. Berman, Guillermo A. Zeballos, Stephen A. Douglas, Herbert B. Tanowitz

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


The potential role of endothelin-I (ET-1) in the pathogenesis of focal microvascular spasm, previously implicated in the etiology of Chagas’ cardiomyopathy, was investigated. There was an increase in ET-1 in the supernatants of Trypanosoma cruzi-infected human umbilical vein endothelial cells (HUVEC). Infection of HUVEC and vascular smooth muscle cells had no effect on the synthesis of transforming growth factor-d, which induces ET-1 synthesis. Bioassay studies of isolated rat aortic rings revealed that the increases in ET-1 production were associated with augmented contractile responses, which were significantly attenuated by preincubation with the ETA receptor antagonist, BQ-123. When big ET was incubated with the parasite, there was no conversion of the precursor to the active hormone (ET-1), demonstrating that the parasite did not possess the necessary converting enzyme. These observations suggest the potential importance of ET-1 in the etiology of the microvascular spasm associated with Chagas’ disease.

Original languageEnglish (US)
Pages (from-to)493-497
Number of pages5
JournalJournal of Infectious Diseases
Issue number2
StatePublished - Feb 1995

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases


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