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Increased activity of guanosine 3′-5′-cyclic monophosphate phosphodiesterase in the renal tissue of cirrhotic rats with ascites

✍ Scribed by Paolo Angeli; Wladimiro Jiménez; Rosalia Veggian; Silvano Fasolato; Roberta Volpin; Harald S. MacHenzie; Raffaella Craighero; Virna Dalla Libera; Antonietta Sticca; Vicente Arroyo; Angelo Gatta

Publisher
John Wiley and Sons
Year
2000
Tongue
English
Weight
136 KB
Volume
31
Category
Article
ISSN
0270-9139

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✦ Synopsis

A possible defect of guanosine 3Ј-5Ј-cyclic monophosphate (cGMP) content in the renal tissue caused by an increased activity of cGMP phosphodiesterase (PDE) has, so far, not been evaluated in the pathogenesis of renal resistance to endogenous natriuretic peptides (ENP) in cirrhosis with ascites. To test this hypothesis the activity of cGMP-PDE and the concentration of cGMP were evaluated in vitro in the renal tissue of 10 control rats and 10 cirrhotic rats with ascites before and after the intravenous (IV) administration of Zaprinast (Sigma, St. Louis, MO), a specific cGMP-PDE inhibitor (30 g/kg/min). Moreover, the effects of the intravenous administration of Zaprinast (15 g/kg/min and 30 g/kg/min) on renal plasma flow (RPF), glomerular filtration rate (GFR), and urinary sodium excretion (U Na V) were evaluated in 10 conscious control rats and 10 conscious cirrhotic rats with ascites. The effects of Zaprinast on plasma renin activity (PRA) was also evaluated in 10 control rats and in 10 cirrhotic rats with ascites. Finally, the effect of Zaprinast on RPF, GFR, and U Na V were evaluated in 10 cirrhotic rats after the IV administration of the ENP-receptor antagonist, HS-142-1. The renal content of cGMP was reduced in cirrhotic rats because of increased activity of cGMP-PDE. Zaprinast inhibited cGMP-PDE activity and increased the renal content of cGMP in these animals. The inhibition of cGMP-PDE was associated with an increase in RPF, GFR, and U Na V and a reduction in PRA. HS-142-1 prevented any renal effect of Zaprinast in cirrhotic rats. In conclusion, an increased activity of the cGMP-PDE in renal tissue contributes to the renal resis-tance to ENP in cirrhosis with ascites. (HEPATOLOGY 2000;31; 304-310.

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