In many species, including swine, fetal plasma glucocorticoids such as cortisol increase as term approaches and are responsible for final maturational changes in numerous tissues (e.g. Silver, 1990; Sangild et al. 1993, 1994; Fowden et al. 1995). On the contrary, excessive exposure to glucocorticoids during gestationmay cause intra-uterine growth retardation, developmental abnormalities or death, or lead to increased incidence of certain diseases during adult life (Blackburn et al. 1965; Reinisch et al. 1978; Seckl et al. 2000). Hence, one might speculate that a closely regulated glucocorticoid exposure is necessary throughout gestation to ensure appropriate development and survival (Klemcke et al. 1999). We have previously demonstrated in pregnant and cyclic pigs that intra-uterine cortisol increases 4- to 6.7-fold between days 10 and 19 of pregnancy (Klemcke et al. 1998). At this time (days 10–19) in conceptus (embryo plus associated extra-embryonic membranes) development, the blastocyst is undergoing quite dramatic changes (Marrable, 1971; Anderson, 1978; Anderson et al. 1993). Part of this development involves the allantois, which rapidly expands between days 18 and 30 owing to water accumulation (Bazer et al. 1981) that might in part result from Na+,K+-ATPase-generated water movement (Macknight & Leaf, 1977). Corticosteroids are known to regulate Na+,K+-ATPase in various tissues (e.g. Verrey et al. 1996)
