Patients with essential hypertension have an impaired endothelium-dependent vascular relaxation in the renal arteries. The possible mechanisms by which essential hypertension is associated with alterations in endothelial function are decreased endothelial nitric oxide (NO) synthase activity, decreased availability or deficiency of L-arginine, increased endogenous NO synthase inhibitor, inactivation of NO by superoxide anions, and increased vasoconstrictors. However, the precise mechanism is not known. In addition, we are now confronted with a difficult question. And the question is whether endothelial dysfunction is a cause or consequence of hypertension. We hypothesize that the initial endothelial dysfunction raises blood pressure, and the development of hypertension impairs much more endothelial function, resulting in constituting the vicious cycle between endothelial dysfunction and hypertension. However, at the moment, it is impossible to answer this question with any certainty. Impairment of endothelial function has been shown to play a critical role in the development and maintenance of hypertension. It is clinically important to select an appropriate intervention that is effective in improving endothelial dysfunction in patients with essential hypertension. Several investigators including us have demonstrated that certain interventions improve endothelial dysfunction of forearm and renal circulation in patients with essential hypertension: angiotensin-converting enzyme inhibitors; lifestyle modification: exercise, body weight reduction, and sodium reduction; estrogen replacement in postmenopausal women; and novel properties: vitamin C and tetrahydrobiopterine. In patients with essential hypertension, endothelial function is impaired in several arteries. However, endothelial dysfunction in essential hypertension is reversible. We can restore endothelial function in essential hypertensive patients.