During hypotonic polyuria renal function studies by the clearance (cl.) method, and urinary PGE2, 6-keto-PGF1 alpha and TxB2 determinations were performed on 14 healthy women in normal potassium balance (N) and 14 healthy women in sustained potassium depletion (KD) induced by low dietary potassium intake (less than or equal to 10 mmol day-1) and natriuretic treatment. By using different depletive patterns, two groups with estimated cumulative potassium deficits of 160 +/- 43 mmol (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. (1) In both the KD1 and KD2 groups as compared to normal potassium balance (N), plasma potassium concentration and urinary potassium excretion were significantly lower; plasma renin activity was significantly higher. (2) Only in KD2 did significant changes appear in renal function and urinary prostanoid excretions. Besides a decrease in creatinine cl. and the urinary flow rate, an increase in fractional chloride excretion and a reduction in distal fractional chloride reabsorption were manifest. The plasma chloride concentration was reduced too. Urinary prostanoid excretions were significantly (6-keto-PGF1 alpha, TxB2) or tendentially (PGE2) lower. (3) Indomethacin treatment resulted in changes in mean arterial pressure (increase) and creatinine cl. (decrease) which were not significantly different in normal potassium balance and KD groups. Only in KD2 did the drug significantly reduce the fractional salt and water excretions and the fractional sodium and chloride deliveries to the diluting segments. However, indomethacin was unable to correct the inhibition of distal fractional chloride reabsorption. Therefore, the potassium depletion attained in the KD2 group was efficacious in depressing renal prostanoid synthesis. This fact, in the presence of high levels of angiotensin II, induced a reduction of the glomerular filtration rate thus contributing to renal ability to retain chloride and potassium.