Effects of maternal captopril treatment on growth, blood glucose and plasma insulin in the fetal spontaneously hypertensive rat

In the spontaneously hypertensive rat (SHR) fetal growth and metabolism are abnormal. It has been speculated that maternal hypertension may be the cau se of these abnormalities. Captopril treatment, which reduces maternal bloo d pressure, during pregnancy and lactation, is reported to have a beneficia l effect postnatally, normalizing the blood pressure of offspring in the SH R. In the present study, the effects of maternal captopril treatment on fet al growth and plasma metabolites were investigated in the fetuses of two ra t strains (SHR and Wistar-Kyoto (WKY)), in order to determine whether norma lizing maternal blood pressure also normalized abnormalities in fetal growt h and metabolism. On fetal Day 20, SHR fetuses were lighter and placentae w ere heavier than for the corresponding WKY. Captopril had no effect on feta l weight in the SHR, but decreased it in the WKY. There was no effect of ca ptopril on placental weight. Fetal plasma insulin levels were higher in the SHR than in the WKY and were decreased by captopril treatment in both stra ins. Fetal blood glucose was elevated and fetal blood lactate was decreased in captopril-treated litters from both strains. Captopril had no effect on fetal plasma IGF-I but fetal plasma IGF-2 levels were lower in the captopr il-treated SHR than in the captopril-treated WKY. These findings suggest th at maternal captopril treatment decreases insulin secretion in the fetal ra t. High levels of fetal plasma insulin suggest that the SHR fetus is insuli n resistant. Fetal insulin levels may contribute to the adverse consequence s of gestational captopril treatment observed in many species. The differen ces in the effect of captopril on the two strains suggest that there are un derlying endocrine differences in the SHR.