Vascular endothelial cells release vasorelaxing factors (endothelium-derived relaxing factor; EDRF), such as nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor (EDHF), and these play an important role in the regulation of vascular tone, vascular permeability and blood coagulation, thus helping to maintain circulatory homeostasis. Preeclampsia is characterized by marked increases in peripheral vascular resistance and vascular permeability together with a disturbance of blood coagulation. It has been suggested that an abnormality in the role played by EDRF in resistance arteries may be involved in the pathogenesis and/or development of preeclampsia. In vitro investigation of characteristic changes in preeclampsia using vascular strips of omental resistance artery obtained from preeclamptic women, revealed that; 1) the action of endothelial NO is reduced not due to decrease in the production of NO in the endothelium but rather to reduced action of guanosine-3,5-cyclic monophosphate (cGMP; a second messenger of NO) itself and/or downstream of cGMP, 2) reduced production of prostacyclin in endothelium and, 3) reservation of EDHF action. Taken together, it was suggested that EDHF might compensate for both the reduced action of endothelial NO and the reduced production of prostacyclin in resistance arteries. In this review the new observation of functional changes in endothelium seen in preeclampsia is important information of obstetricians.