Background. We reported previously that single and 7 d interval repetitive doses of 0.5mg/kg Beta given to pregnant ewes beginning at 104 d gestational age (GA) improved postnatal lung function but caused growth retardation (GR). We did not find GR after ultrasound guided fetal Beta treatments given at later GA. Fetal plasma levels of Beta are 4 fold higher after fetal than maternal Beta treatments. Hypothesis. Fetal Beta begun early in gestation will cause as much or more GR and improvements in postnatal lung function as maternal Beta. Methods. Pregnant ewes with singletons were treated with medroxyprogesterone at 98 d GA and randomized to 5 groups: 1 dose maternal Beta (0.5 mg/kg) at 104 d GA, 1 dose fetal Beta (0.5 mg/kg) at 104 d GA, 3 dose maternal Beta at 104, 111, 118 d GA, 3 dose fetal Beta at 104, 111, 118 d GA, or saline controls that received injections at 104, 111, 118 d GA. 10 to 12 lambs from each group were delivered at 125 d GA. The lambs then were ventilated for 40 min for assessments of postnatal lung function. Results. Mean±SD birth weights for controls (2.7±0.5 kg), 1 dose fetal (2.6±0.3 kg), and 3 dose fetal (2.6±0.2kg) were not different. 1 dose maternal(2.1±0.5 kg) and 3 dose maternal (2.1±0.3 kg) caused equivalent 23% GR (p<0.01). 1 dose fetal did not increase lung compliance, lung gas volume measured at 40cmH2O or alveolar surfactant. 3 dose fetal and 1 dose maternal Beta comparably and significantly increased compliances by 40%, lung volumes by 135%, and alveolar surfactant by about 3 fold relative to control values (p<0.05). 3 dose maternal resulted in larger increases than for all other groups (compliance increased 94%, lung volume increased 300%, alveolar surfactant increased 10 fold) (p<0.01). Conclusions. Maternal Beta improves postnatal lung function more effectively than does fetal Beta and maternal Beta causes GR. This more potent effect of maternal Beta than fetal Beta occurs despite previous information that fetal plasma Beta levels are lower after maternal than after fetal Beta. The results are not consistant with current concepts of how glucocorticoids induce fetal lung maturation and suggest that glucocorticoids mediate fetal maturation, at least in part, via maternal and/or placental responses to the hormone.