Nitric oxide (NO) has been identified as the mediator accounting for the biological effects of endothelium-derived relaxing factor (EDRF) and has been shown to be generated by the action of constitutive and inducible NO-synthases (NOSs) from L-arginine in a variety of cells, including macrophages, neurons and endothelial cells. NO acts as an autocrine or paracrine mediator, its half-life being very short, within the range of few seconds. The NO produced in endothelial cells exerts potent, regional vasodilatatory effects. In the kidney, NO has been shown to play a key role in various processes in normal and pathological conditions. NO is involved in the control of renal basal vascular tone and the maintenance of low vascular resistance. Increasing data suggest that NO interacts with the renin angiotensin system to ultimately influence renal haemodynamic function.