Hypertension is a common public health concern that leads to significant cardiovascular morbidity and mortality worldwide. Blood pressure control is very important in clinical practice to reduce end organ complications such as stroke, myocardial infarction, heart failure, and kidney disease. Untreated hypertension leads to endothelial dysfunction by triggering oxidative stress and a proinflammatory state. Under these conditions, there is increased production of vasoconstrictor prostanoids and reactive oxygen species that cause inactivation of nitric oxide. The reduced nitric oxide bioavailability that characterizes endothelial dysfunction may incite important steps in the appearance and progression of atherosclerotic lesions, including monocyte and leukocyte adhesion, vascular smooth muscle proliferation, and platelet activation. This article will review mechanisms by which persistent endothelial dysfunction directly relates to the development of clinically relevant cardiovascular events. The presence of endothelial dysfunction as indicated by an impaired vasodilatory response to acetylcholine may serve as a marker of future cardiovascular events in patients with essential hypertension. We will also discuss some of the evidence, both experimental and clinical, that available pharmacologic treatment may reverse hypertension-associated endothelial dysfunction. This may represent a new target for therapeutic intervention in essential hypertension.