Mechanism of Fetal Programming Focused on Receptors of Angiotensin
| Project/Area Number |
16591080
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
ITOH Shigeru Juntendo University, Department of Obstetrics and Gynecology, 医学部, 講師 (20296867)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| 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)
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| Keywords | fetal 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 |
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| 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
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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
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Report
(3 results)
Research Products
(3 results)
