Urinary excretion and glomerular synthesis of prostaglandin E2 and prostaglandin F2 alpha in cirrhotic, non-ascitic rats: the effects of sodium overload.
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 PGE2 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.
Santos
J C
JC
Department of Nephrology, Fundación Jiménez Diaz, Madrid, Spain.
Rodríguez-Puyol
D
D
Blanchart
A
A
Hernando
L
L
López-Novoa
J M
JM
D000450:Aldosterone / Q000652:urine; D000818:Animals; D015237:Dinoprost; D015232:Dinoprostone; D007610:Kallikreins / Q000652:urine; D007678:Kidney Glomerulus / Q000378:metabolism*; D008106:Liver Cirrhosis, Experimental / Q000378:metabolism*; D008297:Male; D011458:Prostaglandins E / Q000378:metabolism*; D011460:Prostaglandins F / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000494:pharmacology*
D011458:Prostaglandins E; D011460:Prostaglandins F; D012965:Sodium Chloride; D000450:Aldosterone; D015237:Dinoprost; D007610:Kallikreins; D015232:Dinoprostone