Takimoto E, Ishida J, Sugiyama F, Horiguchi H, Murakami K, Fukamizu A
Institute of Applied Biochemistry and Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Ibaraki 305, Japan.
Science. 1996 Nov 8;274(5289):995-8. doi: 10.1126/science.274.5289.995.
Maternal hypertension is a common complication of pregnancy and its pathophysiology is poorly understood. This phenomenon was studied in an animal model by mating transgenic mice expressing components of the human renin-angiotensin system. When transgenic females expressing angiotensinogen were mated with transgenic males expressing renin, the pregnant females displayed a transient elevation of blood pressure in late pregnancy, due to secretion of placental human renin into the maternal circulation. Blood pressure returned to normal levels after delivery of the pups. Histopathologic examination revealed uniform enlargement of glomeruli associated with an increase in urinary protein excretion, myocardial hypertrophy, and necrosis and edema in the placenta. These mice may provide molecular insights into pregnancy-associated hypertension in humans.
妊娠高血压是妊娠常见的并发症,其病理生理学机制尚不清楚。通过将表达人类肾素 - 血管紧张素系统成分的转基因小鼠进行交配,在动物模型中对这一现象进行了研究。当表达血管紧张素原的转基因雌性小鼠与表达肾素的转基因雄性小鼠交配时,怀孕的雌性小鼠在妊娠后期出现血压短暂升高,这是由于胎盘分泌的人肾素进入母体循环所致。幼崽出生后血压恢复到正常水平。组织病理学检查显示肾小球均匀增大,伴有尿蛋白排泄增加、心肌肥大以及胎盘坏死和水肿。这些小鼠可能为人类妊娠相关高血压提供分子层面的见解。