UA induces endothelial dysfunction not only by reducing the vasodilating NO in the endothelium but also by activating the expression of endothelin-1 (ET-1) and cyclooxygenase-2 (COX-2) in the vascular smooth muscle cells, thereby increasing the production of thromboxane and other vasoconstrictor prostaglandins [19]. This evidence concerns the gene PTGS2 and endothelial dysfunction.