1989 Fiscal Year Final Research Report Summary
PRODUCTION OF ANGIOTENSINOGEN AND KININOGEN IN mRNA LEVEL DURING PREGNANCY
| Project/Area Number |
63570786
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | EHIME UNIVERSITY |
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Principal Investigator |
KITAGAWA Hiroyuki EHIME UNIVERSITY, SCHOOL OF MEDICINE, LECTURER, 医学部, 講師 (60195253)
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| Co-Investigator(Kenkyū-buntansha) |
SHINTANI Toshiaki EHIME UNIVERSITY, SCHOOL OF MEDICINE, ASSISTANT, 医学部, 助手 (50216222)
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| Project Period (FY) |
1988 – 1989
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| Keywords | PREGNANCY / ANGIOTENSINOGEN / KININOGEN / mRNA / SHR |
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| Research Abstract |
(Production of angiotensinogen and kininogen during pregnancy) It has been recognized that renin activity and kininogen concentration are elevated in the blood during pregnancy, although increased in the production of angiotensinogen and kininogen is not yet demonstrated. The present study was conducted to investigate the production of these compounds by using northern blotting analysis. Production of angiotensinogen and kininogen by the liver was more increased in pregnant rats than in non-pregnant rats. Subsequently, the influence of estrogens on increased production of angiotensinogen and kininogen was investigated similarly but using estrogen primed female castrated rats. The production of angiotensinogen and kininogen in estrogen primed female castrated rats was more increased than in only castrated rats significantly. The elevation of estrogens during pregnancy could cause the acceleration of production of angiotensinogen and kininogen in the liver.
(Change of blood pressure and the production of kininogen in pregnant SHR)
In normal rats the constancy of blood pressure was maintained during pregnancy with and without the load of NaCl. While in the spontaneous hypertension rats (SHR) the blood pressure near the termination of pregnancy fell significantly, and the load of NaCl reduced the downward tendency of blood pressure near the termination of pregnancy. In SHRs the acceleration of kininogen production during pregnancy was more marked than in normal rats. The load of NaCl induced the further acceleration of kininogen production on normal pregnant rats, while the load on pregnant SHRs could not induced the further acceleration. The compensation for elevation of blood pressure by the kallikurein-kinin system could be damaged in pregnant SHR.
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