Cyclooxygenase (COX) enzymes catalyse the biotransformation of arachidonic acid to prostaglandins which subserve important functions in cardiovascular homeostasis. Prostacyclin (PGI2) and prostaglandin (PG)E2, dominant products of COX activityin macro- and microvascular endothelial cells, respectively, in vitro, modulate the interaction of blood cells with the vasculature and contribute to the regulation of blood pressure. COXs are the target for inhibition by nonsteroidal anti-inflammatory drugs (NSAIDs--which include those selective for COX-2) and for aspirin. Modulation of the interaction between COX products of the vasculature and platelets underlies both the cardioprotection afforded by aspirin and the cardiovascular hazard which characterises specific inhibitors of COX-2.

Related Organizations

University of Pennsylvania
United States

Keywords

Cyclooxygenase 2 Inhibitors, Heart Diseases, Prostaglandin D2, Receptors, Prostaglandin, Receptors, Epoprostenol, Epoprostenol, Receptors, Thromboxane A2, Prostaglandin H2, Stroke, Thromboxane A2, Prostaglandin-Endoperoxide Synthases, Animals, Eicosanoids, Humans, Endothelium, Vascular, Gastrointestinal Hemorrhage, Isomerases

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