Glucocorticoid activity in the fetal spontaneously hypertensive rat

Abstract

Fetal exposure to high concentrations of corticosteroids in the rat is associated with elevated blood pressure in postnatal life. In this study we have investigated indicators of corticosteroid activity in fetal spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) in order to determine whether fetal corticosteroid exposure is increased in the SHR. Placental 11β-hydroxysteroid dehydrogenase (11β-HSD) activity, which prevents maternal steroids from crossing the placenta, was not impaired in the SHR. Concentrations of amniotic fluid corticosterone were significantly decreased in the SHR compared with the WKY at fetal Day 20, but were not significantly different on fetal Days 16 or 22. This suggests that rather than increased exposure to corticosteroids in the SHR fetus corticosteroid exposure may be reduced. Expression of lung surfactant protein A (Sp-A), a gene induced in late gestation by corticosteroids, was decreased in the SHR. In addition, differences in amniotic fluid electrolyte concentrations were observed which may reflect delayed renal maturation in the fetal SHR. These data suggest that the SHR fetus is exposed to low concentrations of corticosteroids and that the late gestation rise in fetal corticosteroid may be delayed in the SHR.