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Recent reports concerning cardiovascular risk associated with cyclooxygenase\u20102 selective inhibitors have prompted questions about the \u201cprotective\u201d or \u201cdeleterious\u201d role of each COX isoform in cardiovascular disease, and the cloning and expression of inducible PGE\u2010synthase (PGES) open the possibility that PGES could be a new therapeutical target in this context. Predominance of constricting or relaxing prostanoids depends not only on COX activity but also to downstream enzymes such as PGI\u2010synthase (PGIS) and PGES. In the vessel wall, PGIS and PGES seem to be major downstream enzymes in the endothelium and smooth muscle, respectively. Like COX, activity of these enzymes can also be regulated by several factors, which include nitrogen oxides, cytokines, and lipid peroxides. LTs are important inflammatory mediators also involved in the pathophysiology of cardiovascular disease, which are targets for pharmacological intervention. Unlike COX pathway, the biosynthesis of chemotactic and vaso\u2010constrictor LTs in the vasculature strongly depends on leukocyte recruitment and activation, and on cell\u2010cell interaction between leukocytes and vascular cells in the inflamed areas. The present review emphasizes the role of vascular\u2010derived prostanoids and LTs on atherosclerosis. \u00a9 2004 Wiley Periodicals, Inc. 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