Cognitive, Behavioral, and Systems NeuroscienceResearch PaperImportance of central AT1 receptors for sodium intake induced by GABAergic activation of the lateral parabrachial nucleus

The blockade of the inhibitory mechanisms for sodium intake with GABAergic activation in the lateral parabrachial nucleus (LPBN) induces strong ingestion of water and hypertonic NaCl in satiated and normovolemic rats. A question that remains is if the activity of facilitatory mechanisms, like angiotensin II, is necessary for sodium and water intake induced by muscimol (GABAA receptor agonist) injected into the LPBN. Therefore, in the present study, we investigated the effects of the blockade of angiotensinergic AT1 receptors with losartan injected i.c.v. on 0.3 M NaCl and water intake induced by muscimol injected into the LPBN in satiated and normovolemic rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally into the LPBN and unilaterally into the lateral ventricle were used. Bilateral injections of muscimol (0.5 nmol/0.2 μl) into the LPBN combined with i.c.v. injection of vehicle induced 0.3 M NaCl (31.7±1.8 ml/240 min, vs. saline: 0.4±0.3 ml/240 min) and water intake (21.5±1.9 ml/240 min, vs. saline: 0.8±0.2 ml/240 min). Losartan (50 and 100 μg/1.0 μl) injected i.c.v. reduced the effects of LPBN-muscimol on 0.3 M NaCl (18.9±1.9 and 9.9±1.7 ml/240 min, respectively) and water intake (9.8±1.7 and 5.1±1.1 ml/240 min, respectively). The results suggest that the activation of central AT1 angiotensinergic receptors is essential for hypertonic NaCl and water intake induced by the blockade of the inhibitory mechanisms with muscimol injected into the LPBN in satiated and normovolemic rats.

▶Lateral parabrachial nucleus inhibitory mechanisms are essential for sodium satiety. ▶Balance between angiotensin activation and LPBN inhibition results in sodium satiety. ▶ANG II is involved on sodium intake produced by deactivation of inhibitory mechanisms.