Dept. of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Rua Humaitá, 1680, Araraquara, São Paulo, 14801-903, Brazil.
Am J Physiol Regul Integr Comp Physiol. 2011 Jul;301(1):R185-92. doi: 10.1152/ajpregu.00555.2009. Epub 2011 Apr 6.
Lipopolysaccharide (LPS), an endotoxin from the wall of Escherichia coli, produces a general behavioral inhibition and affects several aspects of fluid-electrolyte balance. LPS inhibits thirst; however, it is not clear if it also inhibits sodium appetite. The present results show that LPS (0.3-2.5 mg/kg body wt) injected intraperitoneally produces a dose-dependent reduction of sodium appetite expressed as 0.3 M NaCl intake induced by sodium depletion (furosemide plus removal of ambient sodium for 24 h). The high doses of LPS (1.2-2.5 mg/kg) also produced transient hypothermia at the beginning of the sodium appetite test; however, no dose produced hyperthermia. LPS also increased the stomach liquid content (an index of gastric emptying) after a load of 0.3 M NaCl given intragastrically by gavage to sodium-depleted rats. The α(2)-adrenoceptor antagonist yohimbine (5 mg/kg ip) abolished the effect of LPS on 0.3 M NaCl intake, without changing the effect of LPS on gastric emptying. Injection of RX-821002 (160 nmol), another α(2)-adrenoceptor antagonist, in the lateral cerebral ventricle (LV) also reversed the inhibition of sodium appetite produced by LPS. Yohimbine intraperitoneally or RX-821002 in the LV alone had no effect on sodium intake. Although yohimbine plus LPS produced a slight hypotension, RX-821002 plus LPS produced no change in arterial pressure, suggesting that the blockade of the effects of LPS on sodium intake by the α(2)-adrenoceptor antagonists is independent from changes in arterial pressure. The results suggest an inhibitory role for LPS in sodium appetite that is mediated by central α(2)-adrenoceptors.
脂多糖（LPS），一种来自大肠杆菌细胞壁的内毒素，会导致一般的行为抑制，并影响到几个方面的液体电解质平衡。LPS 会抑制口渴，但目前还不清楚它是否也会抑制钠的食欲。本研究结果表明，LPS（0.3-2.5mg/kg 体重）腹腔注射可剂量依赖性地抑制钠的食欲，表现为通过呋塞米加 24 小时去除环境钠引起的 0.3M NaCl 摄入减少（0.3M NaCl 摄入减少）。高剂量的 LPS（1.2-2.5mg/kg）在钠饥饿测试开始时也会产生短暂的体温过低；然而，没有剂量产生体温过高。LPS 还增加了胃液体含量（胃排空的指标），在胃内给予钠饥饿大鼠 0.3M NaCl 负荷后。α（2）-肾上腺素能受体拮抗剂育亨宾（5mg/kg 腹腔注射）消除了 LPS 对 0.3M NaCl 摄入的影响，而不改变 LPS 对胃排空的影响。在侧脑室内注射 RX-821002（160nmol），另一种 α（2）-肾上腺素能受体拮抗剂，也逆转了 LPS 对钠食欲的抑制。腹腔内注射育亨宾或单独在 LV 中注射 RX-821002 对钠摄入量没有影响。虽然育亨宾加 LPS 产生轻微的低血压，但 RX-821002 加 LPS 对动脉压没有影响，这表明 α（2）-肾上腺素能受体拮抗剂对 LPS 对钠摄入的影响的阻断与动脉压的变化无关。结果表明，LPS 在钠食欲中的抑制作用是通过中枢 α（2）-肾上腺素能受体介导的。
