Chronic consumption of ethanol in adult rats and humans leads to reduced arginine vasopressin (AVP)-producing neurons and prenatal ethanol (PE) exposure has been reported to cause changes in the morphology of AVP-producing cells in the suprachiasmatic nucleus of young rats. The present studies further characterize the effects of PE exposure on AVP in the young adult rat; its hypothalamic synthesis, pituitary storage and osmotically stimulated release. Pregnant rats were fed a liquid diet with 35% of the calories from ethanol or a control liquid diet for days 7 to 22 of pregnancy. Water consumption and urine excretion rate were measured in the offspring at 60 to 68 days of age. Subsequently, the offspring were infused with 5% NaCl at 0.05 ml^.kg^-1.min^-1 with plasma samples taken prior to and at three 40-minute intervals during infusion for measurement of AVP and osmolality. Urine output and water intake were approximately 20% greater in PE-exposed rats than NPE-exposed rats and female rats had a greater water intake than males. The relationship between plasma osmolality and AVP in PE-exposed rats was parallel to, but shifted to the right of, the control rats, indicating an increase in osmotic threshold for AVP release. Pituitary AVP was reduced by 13% and hypothalamic AVP mRNA content was reduced by 35% in PE-exposed rats. Our data suggest that prenatal exposure to ethanol can cause a permanent condition of a mild partial central diabetes insipidus.