In normal pregnancy, early placental development is characterized by the proliferation of villi, a process which is driven by angiogenesis. The trophoblastic enzymes hem oxygenase 1 (Hmox1) and cystathionine γ-lyase (Cth) generate gaseous signalling molecules carbon monoxide (CO) and hydrogen sulphide (H2S), which together with placental growth factor (PlGF), another product of trophoblast, provide a strong proangiogenic effect, also known as “Vascular Protection”. Ahmed and Ramma have proposed that in early onset preeclampsia intrinsic alterations in the biology of the trophoblast lead to an impairment of “Vascular Protection”. Due to an increased secretion of fms like tyrosine kinase 1 as soluble VEGF receptor (sFlt-1) as well as soluble endoglin together with a reduced production of PlGF “Vascular Protection” of normal pregnancy is replaced by “Vascular Dysfunction” of preeclampsia. Adapted from [13].