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• W2034651314 abstract "Lesions of the medial preoptic area in rats cause a transient adipsia and aphagia, with a weight loss of 15–20%. Feeding and drinking behaviours return, with water intakes similar to sham-operated rats. However, the rats remain chronically hypernatremic for a period of at least 2 months. The hypernatremia persists during food deprivation and during stimulation of drinking by extracellular dehydration. No deficiency is evident in urinary concentrating ability or in ability to excrete sodium ions; extrarenal water loss is similar to that of sham-operated rats. The rats do not drink in response to hypertonic saline injection, and they do not retain an imposed water load. A comparison with rats with diabetes insipidus, which avoid hypernatremia by sharply increasing their water intakes, demonstrates that the hypernatremia is related to a dysfunction of intake as well as output. The findings suggest that medial preoptic lesions may reset the set-point for regulation of plasma sodium concentration; they also suggest that the lesions may cause reduced sensitivity to an increase in plasma sodium concentration." @default.
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• W2034651314 date "1976-09-01" @default.
• W2034651314 modified "2023-09-23" @default.
• W2034651314 title "Preoptic hypernatremic syndrome and the regulation of water balance in the rat" @default.
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• W2034651314 doi "https://doi.org/10.1016/0031-9384(76)90110-4" @default.
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