Sodium intake following destruction of the anterior hypothalamus in the rat.
Sodium intake and sodium output were measured in rats before and after lesioning of the anterior hypothalamus. Both parameters were lower than control rats following the lesioning procedure. When an amount of sodium was given orally to these lesioned rats to make up the deficit in sodium intake, no difference was found in sodium intake or output between the rats with lesions and normal rats. Rats with anterior hypothalamic lesions were able to increase their sodium intake following a period of sodium deprivation or adrenalectomy. When presented with concentrations of sodium chloride ranging between 0.9 and 2.5% rats with lesions decreased their intake of sodium in a manner similar to control rats except that the level of intake in the lesioned rats was lower for all concentrations. Control rats and those with lesions were not different in their intakes of KC1 solutions. These findings suggest that the anterior hypothalamus is important in setting the absolute intakes of sodium but does not interfere with the control mechanisms regulating the sodium intake.
D000315:Adrenalectomy; D000818:Animals; D004326:Drinking; D004435:Eating; D007031:Hypothalamus / Q000502:physiology*; D007032:Hypothalamus, Anterior / Q000502:physiology*; D008297:Male; D011189:Potassium Chloride; D051381:Rats; D012964:Sodium / Q000652:urine; D012965:Sodium Chloride; D013997:Time Factors
D012965:Sodium Chloride; D011189:Potassium Chloride; D012964:Sodium