Urinary Excretion and Glomerular Synthesis of Prostaglandin E₂ and Prostaglandin F_2α in Cirrhotic, Non-Ascitic Rats: The Effects of Sodium Overload

Abstract

The urinary excretion of aldosterone, kallikrein and prostaglandin E₂ (PGE₂) 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 PGE₂ was measured in RC rats under the same conditions. Both groups of cirrhotic animals showed a decreased urinary excretion of PGE₂. Isolated glomeruli of RC rats produced less PGE₂than 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.