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expressed in tissues like the kidney or vascular endothe-lium, where it executes important physiological func-tions. COX-2-dependent formation of prostanoids not only results in the mediation of pain or infl ammatory signals but also in the maintenance of vascular integrity. Especially prostacyclin (PGI 2), which exerts vasodilatory and antiplatelet properties, is formed to a signifi cant ex-tent by COX-2, and its levels are reduced to less than half of normal when COX-2 is inhibited. This review outlines the rationale for the development of selective COX-2 in-hibitors and the pathophysiological consequences of se-lective inhibition of COX-2 with special regard to vasoac-tive prostaglandins. It describes coxibs that are current-ly available, evaluates the current knowledge on the risk of atherothrombotic events associated with their intake and critically discusses the consequences that should be drawn from these insights. Copyright © 2005 S. Karger AG, Base