AII occurs in the kidney at concentrations that greatly exceed those accounted for by trapped blood and is unaltered by prior perfusion of the kidneys to remove blood. Furthermore, kidney AII is unaltered by an infusion of AII at rates that double the plasma AII. The converting enzyme blocker SQ 20881 led to a fall in kidney AII and a rise in plasma renin activity (PRA). After dietary sodium deprivation, kidney AII, kidney renin, and PRA were all elevated. Sodium loading depressed plasma and kidney renin but did not alter intrarenal AII. In the two-kidney, one-clip renal hypertension model, kidney AII was elevated in the clipped kidney but unlike kidney renin was not suppressed in the contralateral kidney. Acute renal failure (ARF) induced by uranyl nitrate was associated with raised kidney AII and PRA, whereas no such changes occurred in glycerol-induced ARF. Replacement of volume losses in uranyl-nitrate-treated rats prevented the rise in PRA and the onset of ARF but not the rise in kidney AII. These findings are consistent with a local role of AII in the kidney.