In preeclampsia (PE) and fetal growth restriction (FGR), endothelial dysfunction exists during pregnancy. Affected women are at increased risk for cardiovascular disease throughout life. Increased cardiovascular risk is generally associated with premature aging of the vascular system, particularly the endothelium. It is postulated that PE leads to aging of the endothelium and that a prematurely aged endothelium promotes the development of PE. Premature endothelial aging is often caused by cellular and oxidative stress. An important antioxidant and anti-inflammatory enzyme is heme oxigenase-1 (HO-1). HO-1 expression is induced in endothelial cells (EC) by the NO donor pentaerythrityl tetranitrate (PETN). To date, there is no treatment for PE; however, PETN was used in a clinical trial and was shown to improve maternal clinical outcome. In experimental studies, PETN reduced the effect of oxidative stress in EC. In this project, we will use a cell culture model to investigate whether PE simulating stimuli lead to aging of EC and whether EC aged by oxidative stress respond more strongly to these stimuli. In addition, the effect of PETN in the context of senescence induction will be investigated.