During pregnancy, the renin-angiotensin system (RAS) plays an important role in regulating the markedly expanded circulating blood volume in the uteroplacental circulation. RAS is activated during normal pregnancy; however, blood pressure decreases from the 1st trimester to the 2nd trimester. Vascular responsiveness to angiotensin II (AngII) decreases early in pregnancy; on the other hand, pregnant women who subsequently develop PIH are exquisitely sensitive to the pressor effect of AngII. Interestingly. the maternal circulating RAS and the placental concentration of AngII receptor (ATR) are stable or reduced in PIH. The balance of expression between ATR subtype 1 (AT1) and 2 (AT2) is potentially important in the regulation of vascular tone during pregnancy. Increased AT1/AT2 may explain the loss of vascular refractoriness to AngII in the pathogenesis of PIH. Recently, endothelial progenitor cell (EPC) has been found in the peripheral blood of pregnant women. Although AngII stimulates EPC proliferation, the mobilization is inhibited in PIH. Impairment of EPC mobilization may contribute to insufficient regeneration of endothelium in the impaired utero-placental circulation of PIH. This review focuses on vascular endothelial dysfunction and the effect of RAS in the pathophysiology of PIH.
Keywords: Pregnancy-induced hypertension, renin-angiotensin system, endothelial progenitor cell, aminopeptidase A, angiotensin-(1-7)
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