Sodium excretion in dogs with low-grade caval constriction: role of hepatic nerves.

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.