title: Effects of maternal captopril treatment on growth, blood glucose and plasma insulin in the fetal spontaneously hypertensive rat.
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.
authors: Research Centre for Developmental Medicine and Biology, University of Auckland, New Zealand. rml28@cam.ac.uk
authors: R M
authors: RM
authors: Lewis
authors: M H
authors: MH
authors: Vickers
authors: D C
authors: DC
authors: Batchelor
authors: N S
authors: NS
authors: Bassett
authors: B M
authors: BM
authors: Johnston
authors: S J
authors: SJ
authors: Skinner
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D002216:Captopril / Q000008:administration & dosage / Q000627:therapeutic use*; D004326:Drinking; D005260:Female; D005312:Fetal Blood / Q000737:chemistry / Q000378:metabolism*; D005315:Fetal Diseases / Q000188:drug therapy*; D020567:Fetal Weight; D005865:Gestational Age; D006973:Hypertension / Q000188:drug therapy*; D007328:Insulin / Q000097:blood*; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D007335:Insulin-Like Growth Factor II / Q000032:analysis; D019344:Lactic Acid / Q000097:blood; D008431:Maternal-Fetal Exchange; D009929:Organ Size; D010920:Placenta / Q000033:anatomy & histology; D011247:Pregnancy; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
chemical_list: D001786:Blood Glucose; D007328:Insulin; D019344:Lactic Acid; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II; D002216:Captopril