摘要
The deactivation of the inhibitory mechanisms with injections of moxonidine (伪2-adrenoceptor/imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) increases hypertonic NaCl intake by intra- or extracellular dehydrated rats. In the present study, we investigated the changes in the urinary sodium and volume, sodium balance, and plasma vasopressin and oxytocin in rats treated with intragastric (i.g.) 2 M NaCl load (2 ml/rat) combined with injections of moxonidine into the LPBN. Male Holtzman rats (n=5-12/group) with stainless steel cannulas implanted bilaterally into LPBN were used. Bilateral injections of moxonidine (0.5 nmol/0.2 渭l) into the LPBN decreased i.g. 2 M NaCl-induced diuresis (4.6卤0.7 vs. vehicle: 7.4卤0.6 ml/120 min) and natriuresis (1.65卤0.29 vs. vehicle: 2.53卤0.17 mEq/120 min), whereas the previous injection of the 伪2-adrenoceptor antagonist RX 821002 (10 nmol/0.2 渭l) into the LPBN abolished the effects of moxonidine. Moxonidine injected into the LPBN reduced i.g. 2 M NaCl-induced increase in plasma oxytocin and vasopressin (14.6卤2.8 and 2.2卤0.3 vs. vehicle: 25.7卤7 and 4.3卤0.7 pg/ml, respectively). Moxonidine injected into the LPBN combined with i.g. 2 M NaCl also increased 0.3 M NaCl intake (7.5卤1.7 vs. vehicle: 0.5卤0.2 mEq/2 h) and produced positive sodium balance (2.3卤1.4 vs. vehicle: -1.2卤0.4 mEq/2 h) in rats that had access to water and NaCl. The present results show that LPBN 伪2-adrenoceptor activation reduces renal and hormonal responses to intracellular dehydration and increases sodium and water intake, which facilitates sodium retention and body fluid volume expansion.