Impaired renal response to splanchnic infusion of hypertonic saline in conscious cirrhotic rats
- 1 April 1982
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Renal Physiology
- Vol. 242 (4) , F390-F394
- https://doi.org/10.1152/ajprenal.1982.242.4.f390
Abstract
The renal response to hypertonic NaCl infusion via the portal or the jugular vein, in control rats and in rats in which experimental cirrhosis of the liver was induced, was studied. Cirrhotic rats showed hyponatremia, hypochloremia and hypoproteinemia. Cirrhotic rats excreted 68.8 .+-. 3.8% of the daily Na intake, whereas the excretion in control animals was significantly higher (97.6 .+-. 6.6%). The aim of these experiments was to determine whether the deficit in Na excretion in cirrhotic rats is in some way related to an impaired response to Na loads presented to the portal system. Na and Cl excretion (UNaV, UClV), glomerular filtration rate (GFR), renal plasma flow (RPF) and osmolar excretion (UosMV) were studied in conscious cirrhotic and control rats. The measurements were performed before and after infusion of hypertonic NaCl solution (855 mM at 1.2 ml/h for 30 min) into either a jugular vein or the portal system through the spleen. In the control rats, intrasplenic infusion caused a greater and more rapid rise in UNaV and UClV than i.v. infusion did without changes in GFR and RPF; the changes in packed cell volume in the 2 groups were similar. Basal UNaV and UClV were significantly lower in cirrhotic control animals. After intrasplenic infusion UNaV and UClV were higher than after i.v. infusion, but the maximal increases were lower than in control rats. Apparently, the influence of liver and/or portal system on water and Na excretion by the kidney is blunted but still present in the cirrhotic animals. This might be a partially protective mechanism from water and Na retention, particularly after oral intake.This publication has 10 references indexed in Scilit:
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