Experimentally-induced oligohydramnios (oligo) produces lung hypoplasia. To determine if arginine vasopressin (AVP), a hormone known to decrease fetal lung fluid production, contributes to the pathogenesis of oligo-induced lung hypoplasia, the following experiment was performed. Brattleboro rats were mated to produce litters either with AVP [heterozygotes (HZ)] or without AVP [homozygotes (HO)]. On d 15 of gestation, half of each litter underwent amniocentesis to create persistent oligo. Littermates with intact membranes served as controls. Four groups of fetuses, i.e. 10 HO litters divided into control (44 fetuses) and oligo (25 fetuses), and eight HZ litters divided into control (35 fetuses) and oligo (18 fetuses), were killed at term for measurement of organ weights and biochemical determination of lung development. Significant differences between control and oligo groups were observed for body weight (HO, p = 0.008; HZ, p = 0.03), lung weight (less than 0.001 for both crossings), lung/body weight ratio (less than 0.001 for both), DNA per lung (HO, p = 0.02; HZ, p less than 0.001), and lung dry/wet ratio (HO, p less than 0.001; HZ, p = 0.001). Oligo groups with and without AVP were not found to be different for lung weight (p = 0.217), lung/body weight ratio (p = 0.209), and DNA per lung (p = 0.822). An analysis of variance confirmed the lack of any significant difference of the impact of oligo in the presence or absence of AVP. We conclude that AVP plays no role in the development of oligo-induced lung hypoplasia.