We previously reported that sodium restriction during pregnancy reduces plasma volume expansion and promotes intra-uterine growth restriction (IUGR) in rats while it activates the renin-angiotensin-aldosterone system (RAAS). In the present study, we proceeded to determine whether expression of the two angiotensin II (ANGII) receptor subtypes (AT 1 and AT 2 ) change in relation to maternal water-electrolyte homeostasis and fetal growth. To this end, pregnant (gestation day 15) and non-pregnant Sprague-Dawley rats were randomly assigned to two groups fed either normal, or Na + -restricted diets for 7 days. At the end of the treatment period, plasma aldosterone and renin activity as well as plasma and urine electrolytes were measured. Determinations for AT 1 and AT 2 mRNA and protein were made by RNase protection assay and photoaffinity labelling, respectively, using a number of tissues implicated in volume regulation and fetal growth. In non-pregnant rats, Na + restriction decreases Na + excretion without altering plasma volume, plasma Na + concentration or the expression of AT 1 and AT 2 mRNA or protein in the tissues examined. In normally fed pregnant rats when compared to non-pregnant controls, AT 1 mRNA increases in the hypothalamus as well as pituitary and declines in uterine arteries, while AT 1 protein decreases in the kidney and AT 2 mRNA declines in the adrenal cortex. In pregnant rats, Na + restriction induces a decrease in plasma Na + , an increase in plasma urea, as well as a decline in renal urea and creatinine clearance rates. Protein levels for both AT 1 and AT 2 in the pituitary and AT 2 mRNA in the adrenal cortex are lower in the Na + -restricted pregnant group when compared to normally fed pregnant animals. Na + restriction also induces a decrease in AT 1 protein in the placenta. In conclusion, these results suggest that pregnancy may increase sensitivity to Na