PREVIOUS studies have revealed a close relationship between the prostaglandin (PG) and the renin–angiotensin systems in the kidney^1–4 and we assume that both systems are intimately involved in the regulation of salt and volume homeostasis and of blood pressure. Changes in NaCl and water balance were found to be important determinants of the activity and function of the renin–angiotensin system⁵ and it has been suggested that PG synthesis is also modified by these variables^2,6,7. One factor influencing the pathway and, thus, the consequences of altered PG formation is the enzyme PGE₂-9-ketoreductase, which catalyses the interconversion of the antagonistically acting PGE₂ and PGF_2α (ref. 8). First direct evidence is presented here that PGE₂-9-ketoreductase activity is under the control of NaCl ingestion. We suggest that this enzyme is an important mediator of salt intake-related prostaglandin–renin interaction.