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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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