The objective of this study was to find out if lipopolysaccharide (LPS) administered intraperitoneally affects sodium and water intake and renal excretion in dehydrated rats. LPS (0.3-5 mg/kg b.w.) inhibited 0.3M NaCl intake induced by subcutaneous injection of the diuretic furosemide (FURO, 10 mg/kg b.w.) combined with the angiotensin converting enzyme inhibitor, captopril (CAP, 5 mg/kg b.w.). Only the highest doses of LPS (2.5 and 5 mg/kg) inhibited water intake induced by FURO/CAP. LPS (0.6 mg/kg) reduced urinary volume and sodium excretion, but had no effect on mean arterial pressure or heart rate of rats treated with FURO/CAP. LPS (0.3-5.0 mg/kg) abolished intracellular thirst and reduced by 50% the urine sodium concentration of rats that received 2 ml of 2M NaCl by gavage. LPS (0.3-5.0 mg/kg) also reduced thirst in rats treated with FURO alone (10 mg/rat sc). The results suggest that LPS has a preferential, but not exclusive, inhibitory effect on sodium intake and on intracellular thirst. The inhibition of hydro-mineral intake and the antinatriuresis caused by LPS in dehydrated rats may contribute to the multiple effects of the endotoxin on fluid and electrolyte balance and be part of the strategy to cope with infections.

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 ␣ 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 ␣ 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 ␣ 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 ␣ 2-adrenoceptors. sodium intake; endotoxin; arterial pressure; RX-821002; fluid balance; sickness behavior LIPOPOLYSACCHARIDE (LPS), an endotoxin derived from the wall of gram-negative bacteria, triggers an array of behavioral and systemic responses, grouped under the name of "sickness behavior" (7).Sickness behavior has been hypothesized to be an adaptive syndrome of behavioral and physiological responses by animals coping with infectious pathogens (7). Reduced activity, feeding, and drinking are some of the behavioral alterations induced by infection. These alterations may help to shift internal energy production to increase body temperature and sustain fever, an important mechanism to combat infection.It is possible that the reduced drinking that occurs in sickness behavior is also associated with a general effect on body-fluid balance because LPS releases hormones that influence such balance (4) and reduces several aspects related to sodium metabolism: sodium transport in the gut (5), natriuresis (1, 31), and a rapidly developing sodium intake induced by the diuretic furosemide combined with a low dose of the converting enzyme inhibitor captopril or Furo/Cap (1).In the previous study (1), LPS injected before Furo/Cap treatment inhibited sodium intake produced within 2 h, but it also reduced sodium excretion, which may affect sodium intake. Thus it is not possible to definitively conclude if the inhibition of sodiu...

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