The urinary excretion of aldosterone, kallikrein and prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) was studied in sodium-retaining (RC) and nonretaining (NRC), nonascitic cirrhotic rats, under basal conditions and after an oral sodium load (5 mmol). The glomerular synthesis of PGE<sub>2</sub> was measured in RC rats under the same conditions. Both groups of cirrhotic animals showed a decreased urinary excretion of PGE<sub>2</sub>. Isolated glomeruli of RC rats produced less PGE<sub>2 </sub>than those of the control animals, both under basal conditions and after the sodium load. The NRC group was the only one able to increase the urinary excretion of kallikrein in response to the sodium load. These findings could contribute to explain the early physiopathological events of hepatic cirrhosis.