Low-level direct renal nerve stimulation increases both renal tubular sodium reabsorption and renal renin secretion rate without changing arterial pressure, glomerular filtration rate, renal blood flow, or intrarenal blood flow distribution. The possibility was considered that intrarenal angiotensin II formation might mediate the antinatriuretic effect by directly enhancing renal tubular sodium reabsorption. Low-level direct renal nerve stimulation was performed in anesthetized saline-loaded dogs before and after intrarenal blockade to angiotensin II with [1-sarcosine, 8-alanine]angiotensin II. The antinatriuretic response to low-level direct renal nerve stimulation was not altered by intrarenal blockade to angiotensin II. Renal renin secretion rate was increased by low-level direct renal nerve stimulation in the absence of changes in systemic or renal hemodynamics. The antinatriuretic effect of low-level direct renal nerve stimulation does not depend on the intrarenal action of angiotensin II.