1. The effects of changes in sodium balance on renal prostaglandins have been hitherto studied mainly in experimental animals and the results have been controversial. In this study the 24 h urinary excretion of prostaglandins E2 and F2α was measured by radioimmunoassay in seven normal subjects under basal conditions and after 5 days of a diet containing <20 mmol of sodium/day. Subsequently a sodium chloride (150 mmol/l: saline) load (300 mmol of sodium over 4 h) was infused and prostaglandins were again measured in hourly urine collections. Plasma renin activity and aldosterone were also measured under basal conditions, after the low sodium diet and at 2 and 4 h of the saline infusion.
2. Dietary sodium restriction was associated with a marked increase in prostaglandin E2 excretion (from 769.7 ± 201.6 sem to 1761.3 ± 304.9 ng/24 h, P<0.0005). Prostaglandin F2α also increased from 1187.0 ± 390.1 to 1435.6 ± 344.6 ng/24 h, but this was not statistically significant. The prostaglandin E2/prostaglandin F2α ratio increased from 0.83 ± 0.2 to 1.52 ± 0.34 (P<0.01). Plasma renin activity and aldosterone rose significantly (P<0.05 and<0.0025 respectively).
3. During the saline load prostaglandin E2 decreased after 2 h from 142.4 ± 29.9 to 86.7 ± 22.9 ng/h (P<0.05) and to 36.9 ± 5.96 ng/h after 4 h. Prostaglandin F2α decreased at a slower rate, from 98.4 ± 18.7 to 37.5 ± 8.8 ng/h at 4 h (P<0.02). At 4 h the prostaglandin E2/prostaglandin F2α ratio returned to control values (0.90 ± 0.17). Plasma renin activity and aldosterone decreased significantly after 2 h (P<0.02 and<0.0025 respectively) and reached control values after 4 h.
4. The present study demonstrates that chronic and acute changes in sodium balance induce changes in the excretion of prostaglandin E2 parallel to changes in plasma renin activity and aldosterone. The similar but quantitatively smaller changes in prostaglandin F2α and the inversion of the ratio between the two prostaglandins during sodium deprivation suggest that at least two factors are involved: increased delivery of substrate for prostaglandin synthase and decreased activity of the prostaglandin E2 9-ketoreductase. Prostaglandins probably play an important role in the adaptation of the kidney to changes in sodium balance.