Specific alterations in sodium chloride intake after hypothalamic lesions in the rat

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Abstract
Bilateral electrolytic lesions in the hypothalamus of the rat elicited either a decrease or increase in 2% NaCl intake, without a significant change in water ingestion. Lesions placed in the anterior hypothalamus involving supraoptic or paraventricular nuclei, or both, resulted in a conspicuous fall (as much as 93%) of NaCl intake. The decreased consumption remained to the end of the experiments which in some rats lasted 105 days and was accompanied by a decrease in NaCl urinary output. On the contrary, lesions placed in the central hypothalamus determined a specific increase of NaCl intake together with an augmented urinary excretion. The increased ingestion was permanent and lasted to the end of the experiment, attaining in one rat the value of 290%. To account for these results two provisional explanations are advanced, one of them considering the possibility of the existence of two areas of opposite effects regarding NaCl ingestion and the other claiming a neurohumoral mechanism in which oxytocin and aldosterone could be the two responsible hormones.

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