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Mechanism of Fetal Programming Focused on Receptors of Angiotensin

Research Project

Project/Area Number 16591080
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Embryonic/Neonatal medicine
Research InstitutionJuntendo University

Principal Investigator

ITOH Shigeru  Juntendo University, Department of Obstetrics and Gynecology, 医学部, 講師 (20296867)

Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
Keywordsfetal programming / low protein diet / pregnancy / hypertension / fibrosis of coronary arteries / estrogen / bradykinin / 胎内プログラミング / エストロゲン / ブラジキン / wire myograph
Research Abstract

Objective : Previous reports showed that fetal programming with a dietary protein restriction in pregnant rats causes hypertension in offspring, and that there is a definite distinction between males and females in the incidence of hypertension in adulthood. Therefore, we hypothesized that ovarian dysfunction induced by fetal programming may make hypertension worse and thus impair endothelial function. The aim of this study is to reveal the influence of estrogen on hypertension induced by maternal protein restriction. Method : Wistar rats were fed a diet containing either 18% (group C) or 9% (R) casein throughout pregnancy. The pups were culled to six female pups per litter. Half of the offspring in both the C and R groups were ovariectomized at day 50 (CX, RX), and the other half underwent a sham operation (CO, RO). Blood pressure was measured by tail-cuff plethysmography at days 50, 75, 125, and 175. Between days 175 and 185, the mesenteric arteries were dissected and their vascular … More function was investigated with a wire myograph. Results : Birth weight was not significantly different between C and R. There was no significant difference between the groups in systolic blood pressure on d50 or d75. On d125, RX had significantly higher systolic blood pressure than CX. On d175, blood pressure was higher in R than in C, regardless of the presence of ovaries. There were no differences between R and C rats in their contractile responses to phenylephrine or U46619. The responses to bradykinin were significantly attenuated in RX. Conclusions : This study showed that a maternal low-protein diet during pregnancy induced hypertension in rat offspring without intrauterine growth restriction. In addition, ovariectomized rats developed hypertension earlier than sham-operated rats did. The maternal low-protein diet blunted the vasorelaxation to bradykinin in offspring, and ovariectomy made the attenuation worse. The results also suggested that estrogen is related to the gender difference in hypertension of fetal programming. Less

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (3 results)

All Other

All Journal Article (3 results)

  • [Journal Article] Does estrogen affect the development of abnormal vascular function in offspring of rats fed a low protein diet in pregnancy?

    • Author(s)
      Musha Yuka
    • Journal Title

      Pediatr Res (印刷中)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Does estrogen affect the development of abnormal vascular function in offspring of rats fed a low protein diet in pregnancy?

    • Author(s)
      Musha Yuka, Shigeru Itoh, Katsuyuki Kinoshita
    • Journal Title

      Pediatr Res. (In press)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Does estrogen affect the development of abnormal vascular function in offspring of rats fed a low protein diet in pregnancy?

    • Author(s)
      Musha Yuka
    • Journal Title

      Pediatr Res (印刷中)

    • Related Report
      2005 Annual Research Report

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Published: 2004-04-01   Modified: 2016-04-21  

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