RESUMO
The area postrema (AP) is a circumventricular organ located in the dorsal medulla. Previous studies found that AP lesions lead to increased saline ingestion in the rat. The salt appetite was thought to be a result of primary disruptions in sodium regulation or in cardiovascular regulation. To assess this we measured food and fluid intakes, urinary electrolyte and aldosterone concentration, and blood pressure and heart rates in AP lesioned and control animals during a period of normal sodium intake and during a period of excessive sodium intake. Rats with AP lesions exhibited sodium appetite but not natriuresis. In fact, sodium intake greatly exceeded output. Their urinary aldosterone levels were similar to those of control animals during both periods. The lesioned rats also had lowered heart rates, yet, their blood pressures were similar to control animals. These results are discussed with reference to a possible role of the AP in satiety and in maintaining homeostasis.
Assuntos
Ventrículos Cerebrais/fisiologia , Comportamento de Ingestão de Líquido/fisiologia , Frequência Cardíaca , Bulbo/fisiologia , Equilíbrio Hidroeletrolítico , Aldosterona/urina , Animais , Pressão Sanguínea , Peso Corporal , Eletrólitos/urina , Comportamento Alimentar/fisiologia , Masculino , Vias Neurais/fisiologia , Ratos , Ratos Endogâmicos , Solução Salina HipertônicaRESUMO
Several reports have linked the area postrema (AP), a circumventricular organ in the dorsal medulla, to the control of sodium regulation. To clarify its role further we examined the effects of AP ablations in rats on sodium intake as well as on sodium output. Eighteen experimental rats received lesions to the AP while 6 control rats received sham lesions. After the lesions we gave the animals a two-bottle preference test between water and various molar concentrations of NaCl (0.03, 0.1, 0.3, 0.5), glucose (0.1, 0.3) or KCl (0.1, 0.3) solutions. Rats with AP lesions consumed supranormal amounts of NaCl solutions, but their intakes of glucose and KCl solutions were not significantly different from those of control rats. These changes in intake were apparently not secondary to changes in sodium output. Urinary sodium and potassium levels were the same for both groups of rats while on a normal, sodium-replete diet or on a sodium-free diet. Anatomical analyses revealed a significant correlation between the size of the lesion and the animals' salt intake (NaCl, KCl). Only when the lesions destroyed the AP without appreciable damage to the adjacent nucleus of the solitary tract (NST), a sensory relay for gustatory and visceral afferents, was there a significant tendency for rats to consume more salt solution. These changes in intake cannot be accounted for by lesioned produced deficits in gustatory function. The data were discussed with regard to possible hemodynamic effects of the lesions.