Inhibition of sodium appetite by lipopolysaccharide: involvement of alpha(2)-adrenoceptors
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Data
2011-07-01
Autores
Almeida, R. L. [UNESP]
David, R. B. [UNESP]
Constancio, J. [UNESP]
Fracasso, J. F. [UNESP]
Menani, José Vanderlei [UNESP]
De Luca, L. A. [UNESP]
Título da Revista
ISSN da Revista
Título de Volume
Editor
Amer Physiological Soc
Resumo
Almeida RL, David RB, Constancio J, Fracasso JF, Menani JV, de Luca LA Jr. Inhibition of sodium appetite by lipopolysaccharide: involvement of alpha(2)-adrenoceptors. Am J Physiol Regul Integr Comp Physiol 301: R185-R192, 2011. First published April 6, 2011; doi:10.1152/ajpregu.00555.2009.-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 alpha(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 alpha(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 alpha(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 alpha(2)-adrenoceptors.
Descrição
Palavras-chave
sodium intake, endotoxin, arterial pressure, RX-821002, fluid balance, sickness behavior
Como citar
American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 301, n. 1, p. R185-R192, 2011.