2000 Fiscal Year Final Research Report Summary
Placental CRH and opioid receptor gene expression produced by physical environmental stress and its physiological significance
| Project/Area Number |
11470094
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hygiene
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| Research Institution | Kanazawa University |
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Principal Investigator |
NAKAMURA Hiroyuki Kanazawa University, School of Medicine, Associate professor, 医学部, 助教授 (30231476)
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| Co-Investigator(Kenkyū-buntansha) |
NALAJIMA Madoka Kanazawa University, School of Medicine, Instructor, 医学部, 助手 (10324071)
OGINO Keiki Kanazawa University, School of Medicine, Professor, 医学部, 教授 (70204104)
NAGASE Hirofumi Kanazawa University, School of Medicine, Assistant professor, 医学部, 講師 (00251918)
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| Project Period (FY) |
1999 – 2000
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| Keywords | microwaves / prostaglandin / uteroplacental blood flow / endothelin / CRH / heat / β-endorphin / pregnancy |
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| Research Abstract |
To clarify the involvement of CRH and opioid system in the uteroplacental circulation in the pregnant rats exposed to heat, we examined the effects of heat and intravenous (iv) administration of CRH receptor antagonist α-helical CRH (9-41) on the uteroplacental blood flow (BF) as well as blood CRH, and blood and placental β-endorphin (β EP) in pregnant rats. Heat did not change uterine BF in virgin rats, but reduced uteroplacental BF in pregnant rats. The reduced uteroplacental BF during heat in pregnant rats was reversed by the administration of α-helical CRH.Independent of the status of pregnancy, heat increased blood CRH, which was not reversed by α-helical CRH.Although heat did not change placental βEP, α-helical CRH reduced blood and placenta βEP in pregnant rats. Next, we examined the effects of iv administration of endothelin (ET) receptor antagonist bosentan and a cyclooxygenase inhibitor indomethacin on the uteroplacental BF as well as placental PGE_2 F_<2α> systems in heat exposed or non-heat exposed pregnant rats. The administration of bosentan or indomethacin did not change the uteroplacental BF in non-heat exposed pregnant rats. The administration of bosentan or indomethacin reversed the reduction in the uteroplacental BF during heat. Heat did not change placental PGE_2 system, but increased placental PGF_<2α> system in pregnant rats, which was reversed by bosentan or indomethacin. These results suggest that the uteroplacental circulatory disturbance during heat is mediated by CRH, possibly through the involvement of CRH receptor in rat placenta. The placental opioid system seems unlikely to be involved in the mediation of uteroplacental circulation. The activations of placental ET receptor and PGF_<2α> system seem to be involved in the uteroplacental circulatory disturbances produced by heat. PGF_<2α> system activated by heat may be involved in the vasoconstricting effects of ETA and ETB receptor during heat exposure.
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