We studied the effect of Na + extracellular on Ca 2+ mobilization from intracellular store evoked by carbachol in Trypanosoma cruzi. We report that slow component of Ca 2+ signaling evoked by agonist is dependent on extracellular Na + but not on InsP 3 increase. Moreover, this Ca 2+ signaling progressively increased when pH of the medium changed from 7.0 to 7.8. In addition, we found that it was regulated by PKC. The agonist was also able to induce the alkalinization of the acidic compartment, and both Ca 2+ signaling and alkalinization were inhibited by the EIPA-inhibitor of the Na + /H + exchanger. These results demonstrated the alkalinization of acidic vacuoles and PKC are involved in the triggering of the epimastigote Ca 2+ signaling.
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