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The present results show that LPS (0.3\u20132.5 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\u20132.5 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 \u03b1<jats:sub>2<\/jats:sub>-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 \u03b1<jats:sub>2<\/jats:sub>-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 \u03b1<jats:sub>2<\/jats:sub>-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 \u03b1<jats:sub>2<\/jats:sub>-adrenoceptors.<\/jats:p>","DOI":"10.1152\/ajpregu.00555.2009","type":"journal-article","created":{"date-parts":[[2011,4,7]],"date-time":"2011-04-07T03:21:35Z","timestamp":1302146495000},"page":"R185-R192","source":"Crossref","is-referenced-by-count":9,"title":["Inhibition of sodium appetite by lipopolysaccharide: involvement of \u03b1<sub>2<\/sub>-adrenoceptors"],"prefix":"10.1152","volume":"301","author":[{"given":"R. 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