Abstract
Recent experiments have demonstrated that rats with lesions of the ventral portion of nucleus medianus (vNM) frequently exhibit a chronic and robust hyperdipsia, which occurs only at night. This study indicates that the same brain damage may produce a nocturnal appetite for sodium that is similarly pronounced and persistent. Of 68 rats with vNM lesions, 33 were observed to drink at least 15 ml of 0.51 M NaCl solution per day, and 11 of them consumed more than 30 ml daily. The basis for this impressive consumption of saline is uncertain; the brain-damaged rats had normal sodium concentrations, renin activities, and aldosterone levels in plasma during basal maintenance conditions, and they conserved sodium in urine when maintained on a sodium-deficient diet. Nevertheless, the present results indicate that vNM and/or local fibers of passage may play an important role in the control of sodium appetite, as it does in the control of thirst.
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