To investigate the role of renal prostaglandins (PGs) in the renal handling of sodium, urinary excretion of PGE, PGF2α and PGF2αMUM (main urinary metabolite of PGF2α) were measured after various manipulations of dietary sodium intake in 8 hypertensive patients. A low sodium intake increased urinary excretion of PGF2αMUM (p<0.05), but failed to change urinary excretion of PGE and PGF2α. In contrast, a high sodium intake increased urinary excretion of PGE (p<0.01) and decreased urinary excretion of PGF2αMUM (p<0.02). A low sodium intake decreased the ratio of urinary PGE/PGF2αMUM and a high sodium increased it (both p<0.001). There was a significant positive correlation between urinary excretion of sodium and that of PGE (p<0.001). Additional oral administration of potassium chloride did not change urinary excretion of PGs. These results may suggest that dietary sodium intake may be one of the regulators of the metabolism of PGs in the kidney, supporting the hypothesis that renal PGE has a natriuretic action in humans.
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