Author:
Lewis R. M.,Vickers M. H.,Batchelor D. C.,Bassett N. S,Johnston B. M.,Skinner S. J. M.
Abstract
In the spontaneously hypertensive rat (SHR) fetal growth and metabolism are
abnormal. It has been speculated that maternal hypertension may be the cause
of these abnormalities. Captopril treatment, which reduces maternal blood
pressure, during pregnancy and lactation, is reported to have a beneficial
effect postnatally, normalizing the blood pressure of offspring in the SHR. In
the present study, the effects of maternal captopril treatment on fetal growth
and plasma metabolites were investigated in the fetuses of two rat strains
(SHR and Wistar-Kyoto (WKY)), in order to determine whether normalizing
maternal blood pressure also normalized abnormalities in fetal growth and
metabolism. On fetal Day 20, SHR fetuses were lighter and placentae were
heavier than for the corresponding WKY. Captopril had no effect on fetal
weight in the SHR, but decreased it in the WKY. There was no effect of
captopril on placental weight. Fetal plasma insulin levels were higher in the
SHR than in the WKY and were decreased by captopril treatment in both strains.
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-1 but fetal plasma IGF-2 levels were lower in the captopril-treated
SHR than in the captopril-treated WKY. These findings suggest that maternal
captopril treatment decreases insulin secretion in the fetal rat. High levels
of fetal plasma insulin suggest that the SHR fetus is insulin resistant. Fetal
insulin levels may contribute to the adverse consequences of gestational
captopril treatment observed in many species. The differences in the effect of
captopril on the two strains suggest that there are underlying endocrine
differences in the SHR.
Subject
Developmental Biology,Endocrinology,Genetics,Molecular Biology,Animal Science and Zoology,Reproductive Medicine,Biotechnology
Cited by
6 articles.
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