Previous studies demonstrated the inhibitory participation of serotonergic (5HT) and oxytocinergic (OT) neurons on sodium appetite induced by peritoneal dialysis (PD). The activity of 5HT neurons increases after PD-induced 2% NaCl intake and decreases when the animals are depleted; however, the activity of the OT neurons appeared only after PD-2% NaCl intake. In order to discriminate whether the differential activation of the 5HT and OT neurons in this model is a consequence of the sodium satiation process, or the result of stimulation caused by the entry to the body of a hypertonic sodium solution during sodium access, we analyzed the number of Fos-5HT and Fos-OT immunoreactive neurons in the DRN and the PVN-SON respectively, after isotonic versus hypertonic NaCl intake induced by PD. We also studied the OT plasma levels after PD-induced-isotonic or -hypertonic NaCl intake. PD-induced sodium intake significantly increased the number of Fos-5HT cells, independently of the concentration of NaCl consumed. In contrast, the number of Fos-OT neurons increased after hypertonic NaCl intake, in both depleted and non-depleted animals. The OT plasma levels significantly increased only in PD-2% groups in relation to others, showing a synergic effect of both factors. In summary, 5HT neurons were activated after body sodium status was reestablished, suggesting that this system is activated under conditions of satiety. Regarding the OT system, OT neural activity and OT plasma levels were increased by the entry of hypertonic NaCl solution during sodium consumption, suggesting that this system is involved in the processing of hyperosmotic signals.