| Abstract: | Studied the effects of self-administered iv infusion of hypertonic NaCl, mannitol, glucose, urea, or isotonic NaCl on Na appetite. 22 Merino-Cross sheep were trained to barpress to replace Na deficits of 300–500 mmol. During basal conditions, each delivery to a drinking cup was 15 ml of .6 M NaHCO? (9 mmol). In the experimental situation, an iv infusion was given automatically with each delivery to the drinking cup. Ingestion of NaHCO? solution was significantly reduced by all 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) minutes, irrespective of whether water was concurrently available to drink. At 20 min, plasma Na was increased by hypertonic NaCl, decreased by mannitol or glucose, and not changed by urea. CSF Na concentration was increased by all hypertonic solutions. In regard to the "turn-off" of Na appetite by systemic infusion, 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 suggest that the sensors involved in thirst (e.g., osmoreceptors) are in an area of the brain lacking the blood–brain barrier. (24 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved) |
