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PRODUCTION OF ANGIOTENSINOGEN AND KININOGEN IN mRNA LEVEL DURING PREGNANCY

妊娠期间 mRNA 水平的血管紧张素原和激肽原的产生

基本信息

批准号：
63570786
负责人：
KITAGAWA Hiroyuki
金额：
$ 1.34万
依托单位：
EHIME UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1988
资助国家：
日本
起止时间：
1988 至 1989
项目状态：
已结题

项目摘要

(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.

（妊娠期间血管紧张素原和激肽原的产生）已经认识到，妊娠期间血液中的肾素活性和激肽原浓度升高，尽管尚未证明血管紧张素原和激肽原的产生增加。本研究通过使用北方印迹分析来研究这些化合物的产生。妊娠大鼠肝脏血管紧张素原和激肽原的产生比非妊娠大鼠更多。随后，以类似的方式研究了雌激素对血管紧张素原和激肽原产生增加的影响，但使用雌激素致敏的雌性阉割大鼠。雌激素预处理的雌性去势大鼠血管紧张素原和激肽原的生成量明显高于单纯去势大鼠。妊娠期雌激素水平的升高可引起肝脏血管紧张素原和激肽原的产生加速。妊娠期SHR血压变化及激肽原的产生正常大鼠在妊娠期间，无论是否有NaCl负荷，血压均保持恒定。而自发性高血压大鼠（SHR）在妊娠末期血压明显下降，NaCl负荷可降低妊娠末期血压的下降趋势。在SHR的加速激肽原生产在怀孕期间比正常大鼠更显着。NaCl负荷可进一步促进正常妊娠大鼠激肽原的产生，而妊娠SHR负荷不能进一步促进激肽原的产生。妊娠SHR的激肽释放酶-激肽系统对血压升高的代偿功能可能受损。