• R S Weisinger, D A Denton, and M J McKinley.
• Behav. Neurosci. 1983 Jun 1;97(3):433-44.

AbstractThe effects of self-administered iv infusion of hypertonic NaCl, mannitol, glucose, urea, or isotonic NaCl on Na appetite were studied. Sodium-depleted sheep were trained to bar press in order to replace Na deficits of 300-500 mmol. During basal conditions, each delivery to a drinking cup was 15 ml of .6 M NaHCO3 (9 mmol). In the experimental situation, an iv infusion (10 ml) was given automatically with each delivery to the drinking cup. The ingestion of NaHCO3 solution was significantly reduced by all of the hypertonic solutions, the largest decrease being caused by hypertonic NaCl or mannitol. The decreased intake was observed within 10 (with infusion of hypertonic NaCl, mannitol, or glucose) or 20-40 (with urea infusion) min irrespective of whether water was concurrently available to drink. At 20 min, plasma Na concentration was increased by hypertonic NaCl, decreased by mannitol or glucose, and not changed by urea. Cerebrospinal fluid (CSF) Na concentration was increased by all of the hypertonic solutions. Isotonic NaCl had no effect on the ingestion of NaHCO3 solution, plasma, or CSF composition. In regard to the "turn-off" of Na appetite by systemic infusion, these data are consistent with the theory of neural cells within the blood-brain barrier responsive to changes of Na concentration or osmolality in their environment. In contrast, water intake was stimulated by hypertonic NaCl or mannitol but not by urea or glucose, results suggestive that the sensors involved in thirst (e.g., osmoreceptors) are in an area of the brain lacking the blood-brain barrier.

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