Objective: Preeclampsia (preE), a syndrome of hypertension, and end organ damage, is a leading cause of maternal and fetal morbidity and mortality. Recently, we and other researchers have shown that circulating (pro)renin, soluble (pro)renin receptor (s(P)RR) and placental (P)RR were significantly higher during preE compared to normal pregnancy (NP). In this study, placental expression of (P)RR and serum s(P)RR were evaluated in preE human patients and various rat models of preE. Study Design: (1) Placenta and blood samples were collected from 40 NP and 30 consented preE patients; (2) expression of (P)RR in placenta and soluble (P)RR were evaluated in two established preE rat models: reduced uterine perfusion pressure (RUPP) and deoxycorticosterone acetate (DOCA; PDS) models of preE and were compared to normal pregnant (NP) (SD) rats (n=8). We measured the expression of (P)RR by western blotting (WB) and immunohistochemistry. Plasma (pro)renin and s(P)RR were detected using a commercially available ELISA Kit. Results: The placental expression of (P)RR was higher (p*<0.05) in human preE patients compared to normal pregnant women as evaluated by WB and IHC. The s(P)RR was significantly (p*<0.05) higher in human patients with preE (preE: 31.2 ± 3.15 vs NP:19.6 ± 2.9 ng/mL) . Plasma levels of pro(renin) (normalized to angiotensin I, AngI) (preE: 49.2 ± 10 vs NP: 22.7 ± 4.3 ng/AngI/mL/h) and s(P)RR (preE: 31.2 ± 3.15 vs NP:19.6 ± 2.9 ng/mL) are significantly (p*<0.05; in each case) higher in DOCA rats (PDS) compared to normal pregnant (NP) (*p<0.05). Plasma s(P)RR is significantly (p*<0.05) elevated in RUPP rats (20.06 ± 2.17 ng/mL) compared to NP rats (11.2 ± 2.1 ng/mL). Similarly, plasma (pro)renin is significantly (p*<0.05) elevated in the RUPP group (38.1 + 3.86 (ng/AngI/mL/h) compared to NP rats (21.2 + 3.25 (ng/AngI/mL/h). In the RUPP and DOCA models, both PRR and s(P)RR are approximately doubled compared to controls. Conclusions: These data suggest that increased expression of (P)RR in the placenta and s(P)RR are associated with placental ischemia related to the occurrence of preE in both human patients and animal models of disease.