title: Inhibition of sodium appetite by lipopolysaccharide: involvement of alpha2-adrenoceptors.
abstract: 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.
authors.affiliation: Dept. of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Rua Humaitá, 1680, Araraquara, São Paulo, 14801-903, Brazil.
authors.forename: R L
authors.initials: RL
authors.lastname: Almeida
authors.forename: R B
authors.initials: RB
authors.lastname: David
authors.forename: J
authors.initials: J
authors.lastname: Constancio
authors.forename: J F
authors.initials: JF
authors.lastname: Fracasso
authors.forename: J V
authors.initials: JV
authors.lastname: Menani
authors.forename: L A
authors.initials: LA
authors.lastname: De Luca
mesh_terms: D058669:Adrenergic alpha-2 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D001066:Appetite / Q000187:drug effects* / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001831:Body Temperature / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005746:Gastric Emptying / Q000187:drug effects / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D019329:Idazoxan / Q000031:analogs & derivatives / Q000494:pharmacology; D007274:Injections, Intraperitoneal; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D023421:Models, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D018341:Receptors, Adrenergic, alpha-2 / Q000187:drug effects / Q000502:physiology*; D017673:Sodium Chloride, Dietary / Q000378:metabolism*; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D058669:Adrenergic alpha-2 Receptor Antagonists; D008070:Lipopolysaccharides; D018341:Receptors, Adrenergic, alpha-2; D017673:Sodium Chloride, Dietary; D015016:Yohimbine; C058525:2-methoxyidazoxan; D019329:Idazoxan