1 Stimulation of the renal sympathetic nerves in pentobarbitone anaesthetized rats at low frequencies, which did not statistically change renal blood flow and glomerular filtration rate, significantly reduced urine flow by 35%, absolute sodium excretion by 44% and fractional sodium excretion by 40%. 2 In rats fed a low sodium diet for 2 to 3 weeks, similar renal nerve stimulation caused no consistent changes in renal haemodynamics but decreased urine flow by 38%, absolute sodium excretion by 44% and fractional sodium excretion by 38%, which were identical responses to those obtained in sodium replete animals. In contrast, stimulation of the renal nerves in sodium depleted rats given a constant infusion of captopril at 500 micrograms/kg/h had no statistically significant effect on either water or sodium excretion. 3 Renal nerve stimulation in rats given saline to drink and DOCA for 2 to 3 weeks did not significantly change either renal haemodynamics or the output of water or sodium. However, in other animals maintained on a high salt intake but given a constant infusion of angiotensin II (20 ng/kg/min), renal nerve stimulation caused minimal changes in renal haemodynamics but significantly reduced urine flow by 41%, absolute sodium excretion by 54% and fractional sodium excretion by 49%. 4 These results show that the neurally-mediated tubular responses require the presence of a minimal circulating level of angiotensin II since, when its production is blocked, either acutely or chronically, the renal nerve-induced antinatriuresis and antidiuresis is inhibited but can be restored by the infusion of angiotensin II. These findings provide direct evidence that angiotensin II has an important potentiating action at the renal nerve junctions, most probably at the epithelial cells of the renal tubule.