Studies in normotensive rats showed that excessive fetal exposure to maternal glucocorticoids retards growth and programs hypertension in later life. This excessive exposure is proposed to occur due to a reduction of the placental barrier to maternal glucocorticoids that is provided by 11β-hydroxysteroid dehydrogenase (11βHSD). To assess the possible alterations of glucocorticoid placental barrier in two genetic models of hypertension — spontaneously hypertensive (SHR) and Dahl salt-sensitive rats (DS) and their normotensive counterparts Wistar-Kyoto (WKY) and Dahl salt-resistant rats (DR)—we performed real-time reverse transcriptase–polymerase chain reaction analysis and bioactivity measurements of placental 11βHSD in the last third of gestation. Whereas 11βHSD2 mRNA expression was not different among the investigated strains, 11βHSD1 mRNA abundance was 2.4 times higher in WKY than in SHR and 9.6 times higher in DS than in DR placentae. The 11βHSD2 activity studies performed in placental homogenates revealed activity that did not differ among the strains. Concomitant with 11βHSD1 mRNA expression 11-oxoreductase activity was clearly evident in all strains and was higher in WKY and DS rats than in SHR and DR, respectively. Nevertheless, the net 11βHSD activity of tissue fragments (11β-dehydrogenase minus 11-oxoreductase) was tended toward dehydrogenase action, ie, toward corticosterone inactivation and was significantly lower in DS than in DR rats. The 11β-dehydrogenase/11–oxoreductase ratio was less than 2:1 in SHR and WKY rats, whereas this ratio was 9:1 in DR and 4.5:1 in DS rats. These data suggest that the placental glucocorticoid barrier is not decreased in SHR rats in comparison with normotensive WKY but is lower in DS than in DR counterparts. It cannot be excluded, therefore, that the placental glucocorticoid barrier in Dahl rats influences the pathways that might lead to the sensitivity of blood pressure to high salt intake in later life.