Prenatal dexamethasone causes hypertension in rats when they are studied as adults. While an increase in tubular sodium reabsorption has been postulated to be a factor programming hypertension, this has never been directly demonstrated. The purpose of this study was to examine whether prenatal programming by dexamethasone affected postnatal proximal tubular transport. Pregnant Sprague-Dawley rats were injected with intraperitoneal dexamethasone (0.2mg/kg) daily between 15^th and 18^th day of gestation. Prenatal dexamethasone resulted in an elevation in systolic blood pressure when the rats were studied at 7-8 weeks of age compared to vehicle treated controls, 131 ± 3 vs. 115 ± 3 mm Hg (p<0.001). The rate of proximal convoluted tubule volume absorption, measured using in vitro microperfusion, was 0.61 + 0.07 nl/mm·min in control rats and 0.93+ 0.07 nl/mm·min in rats that received prenatal dexamethasone (p<0.05). Na⁺/H⁺ exchanger activity measured in perfused tubules in vitro using the pH sensitive dye BCECF showed a similar 50% increase in activity in proximal convoluted tubules from rats treated with prenatal dexamethasone. While there was no change in NHE3 mRNA abundance, the predominant luminal proximal tubule Na⁺/H⁺ exchanger, there was an increase in NHE3 protein abundance on brush border membrane vesicles in 7-8-week old rats receiving prenatal dexamethasone. In conclusion, prenatal administration of dexamethasone in rats increases proximal tubule transport when rats were studied at 7-8-week old rats, in part, by stimulating Na⁺/H⁺ exchanger activity. The increase in proximal tubule transport may be a factor mediating the hypertension by prenatal programming with dexamethasone.