The intrarenal pressure was raised to 40--50 mmHg by ureteral occlusion or by renal venous constriction in anesthetized dogs loaded with 10% mannitol in saline and with a urine flow of approximately 1 ml/min/kidney. Both manoeuvres produced vasodilation and decreased urine creatinine excretion (GFR). Ureteral occlusion was associated with a marked antinatriuresis, which contrasted the variable decrements in sodium excretion during renal venous constriction. Ureteral occlusion did not affect urine excretion of kallikrein or kinins, whilst renal venous constriction decreased urinary kallikrein excretion, yet markedly increased urinary kinin excretion. Ureteral occlusion and renal venous constriction comparably increased urine prostaglandin (E-like) excretion by a presumably pressure dependent mechanism. Inhibition of prostaglandin synthesis by indomethacin abolished the vasodilation during renal venous constriction and this was accompanied by marked reductions of urinary creatinine (GFR) and kallikrein excretions, whilst the kinin excretion was enhanced as observed before the administration of indomethacin.