Endothelial dysfunction has been documented both in the forearm and coronary beds of essential hypertensive patients. Impairment in the tonic release of nitric oxide (NO) is secondary to hypertension, while the alteration in agonist-induced endothelium-dependent vasodilation seems to be a primary defect caused both by an alteration of the L-arginine-NO pathway and the production of cyclooxygenase-dependent EDCFs, such as prostanoids or superoxide anions. These latter substances curtail endothelium-dependent vasodilation mainly by inactivating NO production. Although experimental data clearly indicate that the L-arginine-NO pathway participates in the regulation of renal hemodynamics and renal excretory function under basal and stimulated conditions, data in humans are scanty and confounded by methodological approaches. A posteriori interpretation of data obtained with intrarenal infusion of acetylcholine in kidney donors suggests that endothelium dependent vasodilation in the kidney is impaired by aging, a phenomenon well documented in the forearm and coronary circulation. Systemic infusion of L-arginine induced renal vasodilation and natriuresis in normotensive subjects, an effect which seems to be mediated mainly by intrarenal NO production. Moreover the few available data suggest that both renal vasodilation and renal production of NO in response to L-arginine are blunted in patients with essential hypertension and that superoxide anions, may be, at least partially, responsible for this alteration of the L-arginine-NO pathway. In conclusion, endothelial dysfunction has been well documented in the forearm and coronary circulation of patients with essential hypertension. Available data suggest that endothelial, dysfunction is also detectable in the kidney and that a common mechanism, probably superoxide anions, can account for this abnormality.