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Conscious rats received infusions at 5.8 ml./hr of either 0.9% NaCl or 5% dextrose, via a tail vein, for 6 hr. During this infusion period, urine was collected from the animals, and the urine volume, sodium concentration and immunoreactive PGE2 were determined. Urine flow in both groups was stable during the 2-6 hr period of the infusion and was not significantly different between the two groups. Sodium output was also stable over the 2-6 hr infusion period but obviously the output of the saline-infused group was higher than that of the dextrose-infused group. Urinary PGE2 output was not significantly different between the groups in the 2-4 hr period (79.4 +/- 8.6 p-mole/2 hr in the saline-infused group, 82.1 +/- 5.7 p-mole/2 hr in the dextrose-infused group). In the 4-6 hr period, PGE2 output remained at this level (82.0 +/- 7.8 p-mole/2 hr) in the dextrose-infused group, but fell significantly (to 53.7 +/- 5.0 p-mole/2 hr) in the saline-infused group. In separate groups of animals which received saline or dextrose infusions as above, renal papillary osmolality was determined. The osmolality was significantly (P less than 0.001) higher in the saline-infused group. It is concluded that renal PGE2 synthesis is unlikely to be directly involved in sodium homeostasis and that PGE2 synthesis as measured by urinary PGE2 excretion is not controlled by the papillary osmolality.