Growth of Trypanosoma cruzi epimastigotes controlled by shifts in cyclic AMP mediated by adrenergic ligands.

Intracellular levels of cAMP in Trypanosoma cruzi epimastigotes were determined in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, and in the presence of the adrenergic ligand isoproterenol. An increase in the levels of cAMP was observed when those drugs were added. This effect was more pronounced when the cells were in the lag phase of growth. Phosphodiesterase inhibitors, catecholamines and dibutyryl cAMP inhibited proliferation of the organisms, as well as [3H]thymidine incorporation in in vitro experiments. These findings strongly suggest that cAMP plays a role in the control of growth of T. cruzi. The effects of adrenergic ligands in increasing cAMP levels and inhibiting growth could be reversed by beta-adrenergic antagonists, suggesting the presence of a receptor-mediated adenylate cyclase system in T. cruzi. Cholinergic ligands had no effect.