Trypanosoma cruzi infection induces endothelin-1 release from endothelial cells, suggesting a mechanism for the microvascular spasm associated with Chagas' cardiomyopathy.
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ET-1/ETA signaling may contribute to Chagas vasculopathy; leaves open whether antagonists alter cardiomyopathy progression in patients.
Wittner et al. (1995) studied this question.
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