AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 6 1454-R1460, Copyright © 1994 by American Physiological Society
Renal effects of nitric oxide synthesis inhibition in cirrhotic rats
N. M. Atucha, J. Garcia-Estan, A. Ramirez, M. C. Perez, T. Quesada and J. C. Romero
Departamento de Fisiologia, Facultad de Medicina, Murcia, Spain.
In the present study, we have characterized the renal response to
inhibition of endogenous nitric oxide (NO) synthesis [intravenous
NG-nitro-L-arginine methyl ester (L-NAME) for 3 h] in anesthetized
cirrhotic rats, with (ASC) and without (CIR) ascites, at doses that do not
change blood pressure (BP). Administration of L-NAME induced opposite
effects on water (UV) and sodium (UNaV) excretion in cirrhotic and control
animals. Infusion of 1 microgram.kg-1.min-1 of L-NAME in CIR (n = 5)
decreased renal plasma flow (RPF) at the end of the 3-h period, whereas UV,
UNaV, and glomerular filtration rate (GFR) were unaltered. In contrast,
infusion of L-NAME at 10 micrograms.kg-1.min-1 in six more CIR increased UV
and UNaV significantly by the 1st h, without changes in BP or GFR, and
these parameters remained elevated throughout the experiment. Infusion of 1
microgram.kg-1.min-1 in ASC (n = 6) did not change BP or GFR but
significantly enhanced UV and UNaV after the 1st h. These effects were
prevented by pretreatment with L-arginine (0.1 mg.kg-1.min-1) in another
group of ASC infused with 1 microgram.kg-1.min-1 of L-NAME. These results
indicate that, in ASC and CIR cirrhotic rats, inhibition of NO synthesis at
nonpressor does improves renal excretion of sodium and water via a decrease
in tubular reabsorption. NO is an important mediator of the renal excretory
and hemodynamic alterations of experimental liver cirrhosis.
