A new mouse model for pregnancy-induced hypertension.

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Pregnancy-induced hypertension (PIH), the commonest and most serious complications of pregnancy, usually becomes apparent in late pregnancy, the pathophysiology of which has remained elusive (1). Here, we show that later in pregnancy blood pressure is dramatically elevated in transgenic female mice expressing human angiotensinogen only when mated with male mice carrying the human renin gene, which is due to the secretion of feto-placental human renin into the maternal circulation. The observed transient elevation of blood pressure was sharply returned to the non-pregnant state after delivery. Histopathologic examinations revealed uniform enlargement of glomeruli associated with increase in urinary protein excretion, myocardial hypertrophy and necrosis and edema in placenta. These results clearly demonstrate that PIH that caused maternal morbidity and mortality is triggered by the combinatorial action of feto-placental renin genetically derived from male mice with maternal angiotensinogen in transgenic mice.