Participation of alpha(2)-adrenoceptors in sodium appetite inhibition during sickness behaviour following administration of lipopolysaccharide

Autor(es)

De Luca, Jr., Laurival A. ^[1] ; Almeida, Roberto L. ^[2] ; David, Richard B. ^[1] ; de Paula, Patricia M. ^[1] ; Andrade, Carina A. F. ^[1] ; Menani, Jose V. ^[1]

Afiliação do(s) autor(es)

^[1] Sao Paulo State Univ UNESP, Sch Dent, Dept Physiol & Pathol, Sao Paulo - Brazil

^[2] ABC Med Sch, Dept Physiol, Sao Paulo - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: JOURNAL OF PHYSIOLOGY-LONDON; v. 594, n. 6, p. 1607-1616, MAR 15 2016.
• Citações Web of Science: 0

Resumo

Sickness behaviour, a syndrome characterized by a general reduction in animal activity, is part of the active-phase response to fight infection. Lipopolysaccharide (LPS), an effective endotoxin to model sickness behaviour, reduces thirst and sodium excretion, and increases neurohypophysial secretion. Here we review the effects of LPS on thirst and sodium appetite. Altered renal function and hydromineral fluid intake in response to LPS occur in the context of behavioural reorganization, which manifests itself as part of the syndrome. Recent data show that, in addition to its classical effect on thirst, non-septic doses of LPS injected intraperitoneally produce a preferential inhibition of intracellular thirst versus extracellular thirst. Moreover, LPS also reduced hypertonic NaCl intake in sodium-depleted rats that entered a sodium appetite test. Antagonism of (2)-adrenoceptors abolished the effect of LPS on sodium appetite. LPS and cytokine transduction potentially recruit brain noradrenaline and (2)-adrenoceptors to control sodium appetite and sickness behaviour. (AU)

• Processo FAPESP: 03/09857-0 - Mecanismos neuroendócrinos da regulação do eixo hipotálamo-hipófise-adrenal em modelos clínicos e experimentais de resistência aos glicocorticóides e sepse
• Beneficiário: Ayrton Custodio Moreira
• Modalidade de apoio: Auxílio à Pesquisa - Programa PRONEX - Temático
• Processo FAPESP: 11/50770-1 - Mecanismos neurais de regulação do equilíbrio hidroeletrolítico e controle cardiorrespiratório
• Beneficiário: José Vanderlei Menani
• Modalidade de apoio: Auxílio à Pesquisa - Temático