Inhibition of different isoenzymes of cyclooxygenase (COX) and a decrease in prostaglandins at inflammatory sites increase thromboxane A2 (COX-1) and decrease prostaglandin I2 (COX-2) production, which may lead to vasoconstriction, platelet activation, hypertension, accelerated atherosclerosis, renal sodium retention with peripheral edema and heart failure, and increased CV morbidity and mortality [88,92,94,95,96]. This evidence concerns the gene PTGS2 and hypertensive disorder.