PRODUCTION OF ANGIOTENSINOGEN AND KININOGEN IN mRNA LEVEL DURING PREGNANCY

(妊娠期间血管紧张素原和激肽原的产生)人们已经认识到，在怀孕期间血液中的肾素活性和激肽原浓度升高，尽管血管紧张素原和激肽原的产生尚未证实增加。本研究通过Northern印迹分析研究了这些化合物的产生。妊娠大鼠肝脏产生的血管紧张素原和激肽原高于未怀孕大鼠。随后，用雌激素诱导的雌性去势大鼠，类似地研究了雌激素对血管紧张素原和激肽原生成增加的影响。雌激素诱导的去势雌性大鼠血管紧张素原和激肽原的产生明显高于单纯去势大鼠。妊娠期雌激素的升高可引起肝脏血管紧张素原和激肽原生成的加速(妊娠SHR血压变化和激肽原生成)正常大鼠在有无氯化钠负荷的情况下，孕期血压均保持稳定。而自发性高血压大鼠(SHR)终止妊娠时血压明显下降，氯化钠负荷使终止妊娠时血压下降趋势减弱。与正常大鼠相比，SHR孕期激肽原生成的加速更为明显。生理盐水负荷可进一步加速正常妊娠大鼠激肽原的生成，而妊娠SHR负荷不能进一步加速激肽原的生成。激肽释放素激肽系统对血压升高的代偿作用在妊娠高血压综合征中可能受到损害。

(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.