Alteration of the pattern of β-adrenergic desensitization in cultured L₆E₉ muscle cells infected with Trypanosoma cruzi

L₆E₉ myoblasts infected with Trypanosoma cruzi undergo desensitization to β-adrenergic catecholamines in a manner distinct from uninfected control myoblasts. Following incubation of intact cells with isoproterenol for 2h, homogenates prepared from differentiated, high density uninfected L₆E₉ cells retain isoproterenol-dependent adenylate cyclase activity. In addition, previous exposure to isoproterenol is accompanied by a decrease in the number of β-adrenergic receptors. Homogenates of high density L₆E₉ cells infected with T. cruzi retain their adenylate cyclase responsivity to isoproterenol but demonstrate a marked decrease in β-adrenergic receptors. Following desensitization infected cell homogenates lose their responsiveness to isoproterenol and demonstrate a more marked decrease in β-receptors. There does not appear to be any effect of T. cruzi infection on affinity of β-adrenergic agonists for the β-receptor or on changes in agonist affinity associated with desensitization. Infection of low density undifferentiated cells results in no apparent change in adenylate cyclase activity or in β-receptors. Their behavior in the setting of desensitization - decreased whole cell cyclic AMP, decreased adenylate cyclase, unchanged β-receptors - is also not affected by infection. The pattern of desensitization to β-adrenergic agonists in high density infected cells shares several properties with the pattern of desensitization in low density uninfected cells, suggesting that infection may be associated with part of the more primitive cellular response pattern.