AJP - Renal Physiology, Vol 253, Issue 4 672-F678, Copyright © 1987 by American Physiological Society
Sodium excretion in dogs with low-grade caval constriction: role of hepatic nerves
M. Levy and M. J. Wexler
Department of Physiology, McGill University, Montreal, Quebec, Canada.
Low-grade thoracic caval constriction will raise intrahepatic pressure
without driving fluid from the vascular space as ascites. In eight such
dogs where venous pressure was increased by 6.6 cmH2O, sodium balance
studies showed a positive cumulative balance of 85 meq and a weight gain of
480 g over a 6-day period in the absence of any change in renal perfusion,
glomerular filtration rate, central venous pressure, blood pressure,
cardiac output peripheral vascular resistance, or plasma levels of
aldosterone. Liver function tests, including bromosulfophthalein
disappearance curves, were also normal. In dogs with either sham surgery,
or subjected to equivalent venous hypertension of the abdominal vena cava
or portal veins, there was a cumulative positive sodium balance of only
21-28 meq over a 2-day period. When the liver was completely denervated
prior to performing the thoracic caval constriction, the sodium handling
profile reverted to the same pattern as observed in sham controls, i.e., 22
meq cumulative sodium over a 3-day period. When the thoracic caval
constriction was tightened to produce ascites, a LeVeen valve was inserted
and the ascites mobilized. In response to 130 meq/day sodium diet,
denervated dogs excreted the sodium load normally, whereas dogs with intact
hepatic nerves retained sodium and developed anasarca. We conclude that
intrahepatic baroreceptors may modulate sodium excretion in the presence of
intrahepatic hypertension.
