Abstract
Trypanosoma cruzi epimastigote motility can be enhanced by addition of L-arginine, to the culture. This effect is blocked by N-methyl-L-arginine, a competitive inhibitor of the nitric oxide synthase. N-methyl-D-aspartate and L-glutamate, two agonists of the NMDA/L-glutamate receptor, also enhanced motility. This stimulation is blocked by MK-801 a noncompetitive antagonist of the NMDA receptor. In addition, sodium nitroprusside, a guanylyl cyclase stimulator and 8-Br-cyclic GMP, and analog of cyclic GMP, also stimulated epimastigote motility. It is suggested that an increase of intracellular cyclic GMP levels mediated by nitric oxide may be responsible for the increase in epimastigote motility.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acids / pharmacology
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Animals
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Arginine / pharmacology*
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Bucladesine / pharmacology
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Cyclic GMP / analogs & derivatives
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Cyclic GMP / pharmacology
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Dizocilpine Maleate / pharmacology
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Glutamic Acid / pharmacology
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Guanosine Diphosphate / pharmacology
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Guanosine Monophosphate / pharmacology
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Movement / drug effects
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Nitric Oxide / physiology*
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Nitric Oxide Synthase / antagonists & inhibitors
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Trypanosoma cruzi / drug effects
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Trypanosoma cruzi / physiology*
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omega-N-Methylarginine / pharmacology*
Substances
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Amino Acids
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Guanosine Diphosphate
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omega-N-Methylarginine
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8-bromocyclic GMP
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Nitric Oxide
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Glutamic Acid
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Bucladesine
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Dizocilpine Maleate
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Guanosine Monophosphate
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Arginine
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Nitric Oxide Synthase
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Cyclic GMP