A total of 154 patients with essential hypertension (EH), 24 patients with renovascular hypertension (RVH), and 130 Wistar rats were investigated. PGE2 and PGF2 alpha levels were assayed radioimmunologically in renal venous blood and urine of the patients, and the synthesis of PGE2 and PGF2 alpha in renal tissue, renal PGE-9-ketoreductase activity and urinary PG excretion were measured in rats. It was demonstrated that the PGE2 synthesis was depressed in the vascular channel and the renal uropoietic system, with elevated F/E rations, in patients with arterial hypertension. Clinical and experimental studies showed prolonged and excessive salt consumption to be a cause of these changes, rooted in suppressed renal biosynthesis of both PGs and increased conversion of PGE2 to PGF2 alpha. In addition, renal PGE2 inactivation was increased in EH patients, as compared to those with RVH. PGE2 produced in the kidneys of EH patients is always a depressor natriuretic substance, whereas the role of PGF2 alpha is dependent on the water-salt balance. Furosemide and, to a smaller extent, other diuretics, as well as some hypotensive agents, increase urinary PG excretion and depress the F/E ratio in the urine. Repeated PGE2 infusions are shown to enhance the sensitivity of EH patients to hypotensive drugs, so they can be used for the treatment of refractory EH cases.