Document Detail


Effects of maternal captopril treatment on growth, blood glucose and plasma insulin in the fetal spontaneously hypertensive rat.
MedLine Citation:
PMID:  11101275     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
R M Lewis; M H Vickers; D C Batchelor; N S Bassett; B M Johnston; S J Skinner
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Reproduction, fertility, and development     Volume:  11     ISSN:  1031-3613     ISO Abbreviation:  Reprod. Fertil. Dev.     Publication Date:  1999  
Date Detail:
Created Date:  2000-12-06     Completed Date:  2000-12-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8907465     Medline TA:  Reprod Fertil Dev     Country:  AUSTRALIA    
Other Details:
Languages:  eng     Pagination:  403-8     Citation Subset:  IM    
Affiliation:
Research Centre for Developmental Medicine and Biology, University of Auckland, New Zealand. rml28@cam.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / metabolism*
Captopril / administration & dosage,  therapeutic use*
Drinking
Female
Fetal Blood / chemistry,  metabolism*
Fetal Diseases / drug therapy*
Fetal Weight
Gestational Age
Hypertension / drug therapy*
Insulin / blood*
Insulin-Like Growth Factor I / analysis
Insulin-Like Growth Factor II / analysis
Lactic Acid / blood
Maternal-Fetal Exchange
Organ Size
Placenta / anatomy & histology
Pregnancy
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Chemical
Reg. No./Substance:
0/Blood Glucose; 11061-68-0/Insulin; 50-21-5/Lactic Acid; 62571-86-2/Captopril; 67763-96-6/Insulin-Like Growth Factor I; 67763-97-7/Insulin-Like Growth Factor II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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