Transgenic female mice expressing angiotensinogen mated with renin-expressing males developed transient late-pregnancy hypertension and proteinuria due to placental human renin secretion.
A transgenic mouse model expressing human renin and angiotensinogen successfully replicates features of pregnancy-associated hypertension, providing a molecular tool to study this condition.
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.
Takimoto et al. (1996) studied Pregnancy-associated hypertension. Expression of placental human renin and maternal angiotensinogen was evaluated on Blood pressure and histopathologic changes. Transgenic female mice expressing angiotensinogen mated with renin-expressing males developed transient late-pregnancy hypertension and proteinuria due to placental human renin secretion.
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