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Am J Physiol Regul Integr Comp Physiol 278: R917-R923, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 4, R917-R923, April 2000

Effect of hyperosmotic solutions on salt excretion and thirst in rats

G. H. M. Schoorlemmer1, A. K. Johnson1,2,3, and R. L. Thunhorst1,3

Departments of 1 Psychology and 2 Pharmacology and the 3 Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242-1407

We investigated urinary changes and thirst induced by infusion of hyperosmotic solutions in freely moving rats. Intracarotid infusions of 0.3 M NaCl (4 ml/20 min, split between both internal carotid arteries) caused a larger increase in excretion of Na+ and K+ than intravenous infusions, indicating that cephalic sensors were involved in the response to intracarotid infusions. Intravenous and intracarotid infusions of hyperosmotic glycerol or urea (300 mM in 150 mM NaCl) had little or no effect, suggesting the sensors were outside the blood-brain barrier (BBB). Intracarotid infusion of hypertonic mannitol (300 mM in 150 mM NaCl) was more effective than intravenous infusion, suggesting that cell volume rather than Na+ concentration of the blood was critical. Similarly, intracarotid infusion (2 ml/20 min, split between both sides), but not intravenous infusion of hypertonic NaCl or mannitol caused thirst. Hyperosmotic glycerol, infused intravenously or into the carotid arteries, did not cause thirst. We conclude that both thirst and electrolyte excretion depend on a cell volume sensor that is located in the head, but outside the BBB.

natriuresis; blood-brain barrier; urea; mannitol


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