CONTROL OF TRYPANOSOMA-CRUZI EPIMASTIGOTE MOTILITY THROUGH THE NITRIC-OXIDE PATHWAY

Typanosoma cruzi epimastigote motility can be enhanced by addition of L-arginine, to the culture. This effect is blocked by N-omega-methyl-L -arginine, a competitive inhibitor of the nitric oxide synthase. N-met hyl-D-aspartate and L-glutamate, two agonists of the NMDA/L-glutamate receptor, also enhanced motility. This stimulation is blocked by MK-80 1 a noncompetitive antagonist of the NMDA receptor. In addition, sodiu m nitroprusside, a guanylyl cyclase stimulator and 8-Br-cyclic GMP, an analog of cyclic GMP, also stimulated epimastigote motility. It is su ggested that an increase of intracellular cyclic GMP levels mediated b y nitric oxide may be responsible for the increase in epimastigote mot ility.