Introduction : Preeclampsia is an obstetric complication after 20 weeks of pregnancy with a new onset of hypertension and dysfunction of the mother's organs. A decrease in eNOS can trigger an increase in blood pressure as well as a decrease in NO. Vascular endothelial growth factor (VEGF) is not only pro angiogenic but also important in maintaining endothelial and vascular health. Pravastatin can inhibit the activity of Hydroxymethylglutarate-Coa Reductase (HMG-CoA) thereby activating eNOS and producing Nitrite Oxcide (NO). Nitrite Oxcide (NO) serves as a vasodilator for angiogenic balance. Materials and Methods : This research design uses true experimental design with post test only control group design. The current study was conducted in vivo using stored biological material of liver organ tissue of pregnant rats (Rattus norvegicus) wistar strain model of preeclampsia with 3 different doses of pravastatin, namely 2 mg / KgBB, 4 mg / KgBB, and 8 mg / KgBB. VEGF expression, eNOS were observed in this study. Result : Pravastatin doses of 2, 4, and 8 mg/kg increased VEGF and eNOS in the treatment group compared to positive controls. Anova's tests on VEGF (p=0.015) and eNOS (p=0.000) expressions confirmed the hypothesis. The correlation test showed a difference in VEGF expression (p-value 0.006; r = 0.594) and eNOS (p-value 0.000; r = 0.856) between pravastatin dose and VEGF and eNOS expression there was a significant and positive direction, where the higher the dose of pravastatin, the expression of VEGF and eNOS increased. The optimal dose of VEGF and eNOS at a dose of 8 mg/kgBB. Conclusion : Pravastatin has been shown to increase VEGF and eNOS expression in a rat model of liver preeclampsia.