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Department of Physiology and Pharmacology, Medical School, Queen's Medical Centre, Nottingham.

1. Intakes and urine outputs of fluid and electrolytes were measured before, during and after water deprivation in normal rats (Long-Evans strain) and in vasopressin-deficient rats (Brattleboro strain). 2. In a parallel experiment it was confirmed that the water-deprivation schedule used (Long-Evans rats 53 h, Brattleboro rats 14 h), and previously shown to cause similar percentage reductions in plasma volumes in the two strains, did produce more marked hypernatraemia and hyperosmolality and a greater percentage reduction in body weight in Brattleboro than in Long-Evans rats. 3. In Long-Evans rats, water deprivation caused a gradual reduction in urine output, a reduction in food intake and, during the first 24 h, increases in Na+ and K+ output. In Brattleboro rats, the reduction in urine output was more pronounced, but despite this total water losses were greater than from Long-Evans rats. Brattleboro rats showed a greater reduction in food intake. Their urinary Na+ and K+ losses were elevated during the first 9 h of water deprivation; thereafter these variables fell but remained above the level of intake. 4. The cumulative Na+ losses during water deprivation were similar in the two strains but the cumulative K+ losses in the Brattleboro rats were greater than in the Long-Evans rats. Thus the relative hypernatraemia and hyperkalaemia in water-deprived Brattleboro rats compared to water-deprived Long-Evans rats cannot be explained simply on the basis of differences in renal fluid and electrolyte handling. 5. There were significant increases in plasma angiotensin II and aldosterone levels at the end of the water deprivation periods in both strains of rat, and after the drinking water was returned there was a marked anti-natriuresis consistent with an expression of one of the renal actions of aldosterone.

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