We investigated the effects of α- and β-adrenergic receptor agonists on the ability of Toxoplasma gondii to infect and proliferate in cultured murine macrophages. Macrophages pretreated in vitro with varying concentrations of α- and β-adrenergic agonists and incubated with the RH strain of T. gondii did not result in a significant increase in the percentage of infected macrophages compared with negative controls. When parasites were pretreated with l-phenylephrine, an α-agonist, and l-isoproterenol, a β-agonist, before infection, there was no significant change in the percentage of infected macrophages. Clonidine, an α2-adrenergic agonist, led to a significant decrease in the number of infected macrophages at all concentrations tested. The effects of clonidine were blocked by yohimbine, a specific α2-adrenergic antagonist, but not by phentolamine, an α1-adrenergic antagonist. These results suggest that the antiparasitic effects exhibited by clonidine (α2-adrenergic agonist) are mediated through an α2-adrenoreceptor found on the surface of T. gondii.
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