Inhibitory mechanisms in the lateral parabrachial nucleus (LPBN) and central GABAergic mechanisms are involved in the regulation of water and NaCl intake. Besides increasing fluid depletion-induced sodium intake, the activation of GABA A receptors with muscimol into the LPBN also induces ingestion of 0.3 M NaCl in normonatremic, euhydrated rats. It has been suggested that inhibitory mechanisms activated by osmotic signals are blocked by GABA A receptor activation in the LPBN, thereby increasing hypertonic NaCl intake. Therefore, in the present study we investigated the effects of muscimol injected into the LPBN on water and 0.3 M NaCl intake in hyperosmotic cell-dehydrated rats (rats treated with an intragastric load of 2 M NaCl). Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. In euhydrated rats, muscimol (0.5 nmol/0.2 μl), bilaterally injected into the LPBN, induced ingestion of 0.3 M NaCl (24.6 ± 7.9 vs. vehicle: 0.5 ± 0.3 ml/180 min) and water (6.3 ± 2.1 vs. vehicle: 0.5 ± 0.3 ml/180 min). One hour after intragastric 2 M NaCl load (2 ml), bilateral injections of muscimol into the LPBN also induced 0.3 M NaCl intake (22.1 ± 5.2 vs. vehicle: 0.9 ± 0.8 ml/210 min) and water intake (16.5 ± 3.6 vs. vehicle: 7.8 ± 1.8 ml/210 min). The GABA A antagonist bicuculline (0.4 nmol/0.2 μl) into the LPBN reduced the effect of muscimol on 0.3 M NaCl intake (7.1 ± 2.1 ml/210 min). Therefore, the activation of GABA A receptors in the LPBN induces ingestion of 0.3 M NaCl by hyperosmotic cell-dehydrated rats, suggesting that plasma levels of renin or osmolarity do not affect sodium intake after the blockade of LPBN inhibitory mechanisms with muscimol.