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?(Fig.11B). Plasma sFlt-1 levels and arterial pressure responses in NP and RUPP pregnant rats Placental ischemia in pregnant rats significantly increased mean arterial pressure (139?��?2?mmHg, n?=?8, P?GS-7340 manufacturer the hypertension, plasma sFlt-1 concentrations increased approximately threefold when compared with NP control rats (3431?��?454, n?=?8 vs. 1432?��?255?pg/mL, n?=?10 P?BIBF1120 Losartan (10?mg/day for 5?days in drinking water). Data expressed as mean?��?SEM. ... Effect of AT1 receptor blockade on plasma sFlt-1 levels in response to reductions in uterine perfusion pressure in pregnant rats Treatment with Losartan (10?mg/day for 5?days), an AT1 receptor antagonist, significantly reduced the hypertension in response to placental ischemia (113?��?2?mmHg, n?=?9, P?Adenylyl cyclase thought to be the result of an increased circulating concentration of anti-angiogenic factors, such as sFlt-1, and subsequent reductions in pro-angiogenic factors, such as VEGF and PlGF (Wang et?al. 2009). During normal pregnancy, the balance between pro- and anti-angiogenic factors is tightly regulated. However, during PE, this regulation is lost and there is an over production of placental sFlt-1 (Nagamatsu et?al. 2004; Nevo et?al. 2006; Makris et?al. 2007) by mechanisms yet to be fully elucidated. Involvement of the renin�Cangiotensin system in the pathogenesis of preeclampsia has been suggested. Recent data demonstrate the placenta houses its own RAS, independent of the renal RAS (Herse et?al. 2008; Irani and Xia 2008), and the two may have a reciprocal relationship during PE, such that when the uterine RAS is increased, the renal and systemic RAS are decreased (Shah 2005).