Intrauterine growth retardation (IUGR) is characteristic of the fetal alcohol syndrome (FAS). This IUGR is partly due to the toxic effect of ethanol upon placental function, including amino acid transport. Amino acid transport is dependent, in part, upon Na,K-ATPase; therefore, plasma membrane activity of Na,K-ATPase was measured in rat placentas following acute or chronic ethanol exposure. Acute (A) animals were chow fed and gavaged with ethanol on day 20 of gestation and killed 2 hr later; controls (A-C) received sucrose. Binge (B) animals were gavaged on gestation days 18 and 19; controls (B-C) received sucrose. Chronic animals were fed ethanol in a liquid diet containing 2% (CHR-2%) or 6% (CHR-6%) ethanol by volume and killed on day 20. Controls (CHR-2%-C or CHR-6%-C) were isocalorically pair fed. Maternal blood ethanol levels were 197.1 +/- 29.7 mg/dl (mean +/- SE) for A dams and 128.2 +/- 15.2 for B (drawn at time of death); 12.6 +/- 2.2 for CHR-2% and 195.0 +/- 26.0 for CHR-6% (drawn weekly and at time of death). Placental weight was increased and fetal weight decreased in the CHR-6% animals. A, B, and CHR-2% placental and fetal weights were unaffected. Na,K-ATPase specific activity was increased in B placentas: B = 134.7 +/- 16.5 versus B-C = 50.0 +/- 7.4 nmol of Pi/mg of protein/min (p less than 0.01). Conversely, CHR-6% treatment diminished enzyme activity: CHR-6% = 37.0 +/- 4.5 versus CHR-6%-C = 58.5 +/- 4.4 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)