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Am J Physiol Regul Integr Comp Physiol 281: R1368-R1373, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 5, R1368-R1373, November 2001

Mice deficient in oxytocin manifest increased saline consumption following overnight fluid deprivation

Janet A. Amico1,2,3, Mariana Morris4, and Regis R. Vollmer2

1 Department of Medicine, School of Medicine, 2 Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, 3 Department of Veterans Affairs Medical Center, Pittsburgh, Pennsylvania 15261; and 4 Department of Pharmacology and Toxicology, Wright State University School of Medicine, Dayton, Ohio 45401-0927

Male mice (9-13 mo of age) in which the gene for oxytocin (OT) had been deleted (OT -/-) were administered 0.5 M sodium chloride (NaCl) solution or tap water as a two-bottle choice test following overnight fluid deprivation (1600 to 1000 the following day). Compared with wild-type cohorts (OT +/+), OT-deficient mice ingested sevenfold greater amounts of saline in the first hour following reintroduction of fluids, P < 0.001, and fourfold greater amounts at the end of 6 h, P < 0.02. No significant difference in total water ingested was noted between the two genotypes at the end of either 1 or 6 h. If food deprivation accompanied the overnight fluid deprivation and food was reintroduced 1 h after the reintroduction of both water and saline, OT -/- mice still ingested greater amounts of saline, but not water, than OT +/+ mice at both 1 h, P < 0.001, and 6 h, P < 0.02. No differences were noted between genotypes in the daily intake of 0.5 M NaCl solution or water during a 3-day observation period before the overnight fluid deprivation. The volume of saline consumed in each 24-h observation period represented about one-tenth of the total fluids ingested in each genotype. We conclude that OT -/- mice display an enhanced salt appetite compared with OT +/+ mice when fluid deprived overnight. The salt appetite was only apparent in the presence of a perturbation such as fluid deprivation, which predisposes the animal to moderate hypovolemia. The observations support an inhibitory role for OT in the control of sodium appetite in mice.

hypovolemia; neurohypophysis; osmoregulation; posterior pituitary


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