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The stimulation of thromboxane/endoperoxide receptors (TP) elicits diverse physiological/pathophysiological reactions, including platelet aggregation and contraction of vascular smooth muscle. Furthermore, the activation of endothelial TP promotes the expression of adhesion molecules and favors adhesion and infiltration of monocytes/macrophages. In various cardiovascular diseases, endothelial dysfunction is predominantly the result of the release of endothelium-derived contracting factors that counteract the vasodilator effect of nitric oxide produced by the endothelial nitric oxide synthase. Endothelium-dependent contractions involve the activation of cyclooxygenases, the production of reactive oxygen species along with that of endothelium-derived contracting factors, which diffuse toward the vascular smooth muscle cells and activate their TP. TP antagonists curtail the endothelial dysfunction in diseases such as hypertension and diabetes, are potent antithrombotic agents, and reduce vascular inflammation. Therefore, TP antagonists, because of this triple activity, may have a unique potential for the treatment of cardiovascular disorders.