AJP - Gastrointestinal and Liver Physiology, Vol 260, Issue 6 972-G976, Copyright © 1991 by American Physiological Society
Enhanced responsiveness to CNS-induced natriuresis in anesthetized nonascitic cirrhotic rats
I. Colina, J. Quiroga, F. Guarner, A. Purroy and J. Prieto
Department of Medicine, University of Navarra, Pamplona, Spain.
Central nervous system (CNS)-induced natriuresis was investigated in
nonascitic rats with CCl4-induced cirrhosis (CTC rats) under pentobarbital
anesthesia. At baseline, urine sodium output (UNa+V, in mumol.min-1.100 g
body wt-1) (-30%, P less than 0.01) and mean arterial pressure (MAP, in
mmHg) (-12%, P less than 0.001) were significantly reduced in CTC rats (n =
32) compared with matched controls (n = 34). In response to
intracerebroventricular infusion of sodium-rich (349 mM) artificial
cerebrospinal fluid (Na(+)-CSF infusion), UNa+V was significantly higher in
CTC rats (2.8 +/- 0.3; n = 15) than in controls (1.7 +/- 0.2; n = 17; P
less than 0.01); no differences were found in pressor changes (24 +/- 3 vs.
19 +/- 2). A similar but normal sodium CSF (150 mM) infusion did not
influence UNa+V or MAP in any group (n = 12, both). In contrast, CTC rats
(n = 5) showed, compared with controls (n = 5), significantly reduced
natriuretic (UNa+V, 6.9 +/- 0.5 vs. 12.4 +/- 0.9; P less than 0.001) and
pressor (+16 +/- 3 vs. +31 +/- 2; P less than 0.01) responses to an
intravenous hypertonic sodium overload. Natriuresis induced by Na(+)-CSF
infusion was related to increases in creatinine clearance (similar in both
groups) and in fractional sodium excretion, which was significantly higher
in CTC rats (5.90 +/- 0.15%) than in controls (3.65 +/- 0.14%; P less than
0.01). In summary, CNS-dependent efferent natriuretic mechanisms were
preserved in CTC rats and were able to reverse renal tubular sodium
retention in these animals. It is proposed that Na(+)-CSF infusion may be a
useful tool for the study of renal sodium retention in experimental liver
cirrhosis.
