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AJP - Regulatory, Integrative and Comparative Physiology, Vol 269, Issue 5 1085-R1092, Copyright © 1995 by American Physiological Society
ARTICLES |
F. S. Kraly, Y. M. Kim, L. M. Dunham and R. A. Tribuzio
Department of Psychology, Colgate University, Hamilton, New York 13346, USA.
Drinking after intragastric hypertonic solutions was examined to determine whether increased plasma osmolality always accompanied initiation of drinking. A 2-ml infusion through a gastric catheter was the beginning of tests in Sprague-Dawley male rats. Latency to drink was shorter and 1-h water intake was greater for increasing concentrations of NaCl (600, 1,200, and 1,800 mosmol/kg) compared with baseline (290 mosmol/kg). Although 600, 900, or 1,200 mosmol/kg NaCl elicited drinking, such infusions failed to change systemic plasma osmolality, and 900 mosmol/kg also failed to change plasma sodium, protein, renin activity, or packed cell volume at the initiation of drinking. Intragastric 900 mosmol/kg sodium bicarbonate, sodium isethionate, potassium chloride, lithium chloride, and mannitol differentially increased water intake. Total subdiaphragmatic vagotomy abolished drinking elicited by intragastric NaCl; selective gastric or hepatic vagotomy attenuated intake under some conditions. These results support the hypothesis of a vagally mediated, gastrointestinal and/or hepatic-portal, osmosensitive mechanism for initiation of drinking in advance of postprandial increases in systemic osmolality.
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