Endothelial cells are an important source for eicosanoid formation in the cardiovascular system. All of the major pathways of eicosanoid production have been demonstrated in endothelial cells, yielding significant amounts of prostacyclin (PGI2), PGE2, PGF2 alpha, thromboxane A2, leukotrienes and a number of hydro-(pero)xy fatty acids. The regulation of eicosanoid production by endothelial cells is poorly understood. There is evidence that precursors, such as arachidonic acid, may be provided by other cell types. Endothelial cell-derived eicosanoids are involved in the regulation of local vessel tone, intravascular platelet activation, cell locomotion and, eventually, cell proliferation. Most of the available information today considers prostacyclin. This compound is the quantitatively dominating eicosanoid in endothelial cells. Major actions of PGI2 include inhibition of platelet activation and aggregation, relaxation of arterial vessels and inhibition of growth-factor release. There is probably a tight interaction with other biologically active mediators which needs further evaluation. The unique property of the eicosanoid system to become activated only in response to stimulation, the local nature of this reaction, the multiplicity of products formed and the short half-life of most of them are currently the most significant obstacles to define the role of endothelial cell-derived eicosanoids in clinical practice.