Andrade Carina A F, De Luca Laurival A, Colombari Débora S A, Menani José V
Department of Physiology and Pathology, School of Dentistry, UNESP, Rua Humaitá 1680, Araraquara 14801-903, SP, Brazil.
Behav Brain Res. 2007 Nov 2;183(2):156-60. doi: 10.1016/j.bbr.2007.06.003. Epub 2007 Jun 12.
alpha2-Adrenoceptor activation with moxonidine (alpha2-adrenergic/imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) enhances angiotensin II/hypovolaemia-induced sodium intake and drives cell dehydrated rats to ingest hypertonic sodium solution besides water. Angiotensin II and osmotic signals are suggested to stimulate meal-induced water intake. Therefore, in the present study we investigated the effects of bilateral injections of moxonidine into the LPBN on food deprivation-induced food intake and on meal-associated water and 0.3M NaCl intake. Male Holtzman rats with cannulas implanted bilaterally into the LPBN were submitted to 14 or 24h of food deprivation with water and 0.3M NaCl available (n=6-14). Bilateral injections of moxonidine (0.5nmol/0.2microl) into the LPBN increased meal-associated 0.3M NaCl intake (11.4+/-3.0ml/120min versus vehicle: 2.2+/-0.9ml/120min), without changing food intake (11.1+/-1.2g/120min versus vehicle: 11.2+/-0.9g/120min) or water intake (10.2+/-1.5ml/120min versus vehicle: 10.4+/-1.2ml/120min) by 24h food deprived rats. When no food was available during the test, moxonidine (0.5nmol) into the LPBN of 24h food-deprived rats produced no change in 0.3M NaCl intake (1.0+/-0.6ml/120min versus vehicle: 1.8+/-1.1ml/120min), nor in water intake (0.2+/-0.1ml/120min versus vehicle: 0.6+/-0.3ml/120min). The results suggest that signals generated during a meal, like dehydration, for example, not hunger, induce hypertonic NaCl intake when moxonidine is acting in the LPBN. Thus, activation of LPBN inhibitory mechanisms seems necessary to restrain sodium intake during a meal.
将莫索尼定（一种α2 - 肾上腺素能/咪唑啉受体激动剂）注入外侧臂旁核（LPBN）激活α2 - 肾上腺素能受体，可增强血管紧张素II /低血容量诱导的钠摄入，并驱使细胞脱水的大鼠除了饮水外还摄取高渗氯化钠溶液。血管紧张素II和渗透信号被认为可刺激进餐诱导的饮水。因此，在本研究中，我们研究了双侧向LPBN注射莫索尼定对食物剥夺诱导的食物摄入以及与进餐相关的水和0.3M氯化钠摄入的影响。将双侧植入LPBN插管的雄性霍尔茨曼大鼠禁食14或24小时，同时提供水和0.3M氯化钠（n = 6 - 14）。双侧向LPBN注射莫索尼定（0.5nmol / 0.2微升）可增加与进餐相关的0.3M氯化钠摄入量（11.4±3.0毫升/ 120分钟，而注射溶媒组为：2.2±0.9毫升/ 120分钟），但对禁食24小时大鼠的食物摄入量（11.1±1.2克/ 120分钟，而注射溶媒组为：11.2±0.9克/ 120分钟）或水摄入量（10.2±1.5毫升/ 120分钟，而注射溶媒组为：10.4±1.2毫升/ 120分钟）没有影响。当测试期间没有食物时，向禁食24小时大鼠的LPBN注射莫索尼定（0.5nmol）对0.3M氯化钠摄入量（1.0±0.6毫升/ 120分钟，而注射溶媒组为：1.8±1.1毫升/ 120分钟）和水摄入量（0.2±0.1毫升/ 120分钟，而注射溶媒组为：0.6±0.3毫升/ 120分钟）均无影响。结果表明，进餐期间产生的信号，如脱水，而非饥饿，在莫索尼定作用于LPBN时会诱导高渗氯化钠摄入。因此，激活LPBN抑制机制似乎是抑制进餐期间钠摄入所必需的。
