Evidence for an Hepatic Role in the Control of Sodium Excretion 1

Abstract

Discussion and Conclusions

The increased natriuresis found after a small hypertonic sodium chloride load was infused into anesthetized dogs was found to be greater when the stimulus was administered directly into the hepatic circulation than when it was infused systemically via the femoral vein. In addition, the response appears to be dose-related within limits. At 0.05 ml/kg/min a significant natriuresis was obtained only after portal loading. At double this rate, significant increases in sodium excretion occurred with both routes of administration, but the increase after portal loading was more than 50% greater. At a higher rate of infusion (0.4 ml/kg/min) no difference was observed between routes. It would appear that the liver exerts a modest influence on sodium excretion and that the modest contribution of an hepatic component is obscured by other components of the natriuretic response to saline loading when the load of saline is increased.

Data obtained when 5% saline was infused distal to the hepatic circulation into the right atrium indicate no difference from systemic loading. Since an infusion rate was used (0.1 ml/kg/min) which resulted in a difference when infused via the portal vein, these experiments provide additional support for the involvement of the liver in the natriuretic response.

Substitution of a 56% sucrose solution, isosmotic with 5% sodium chloride, resulted in no difference between portal and femoral infusion when infused at 0.1 ml/kg/min for 30 min. Thus, the liver would appear to be responsive to an increase in sodium concentration rather than to an increase in osmolality in the portal blood.

Daly et al., using similar stimulus parameters, reached similar conclusions by means of a different experimental design. Although our experiments were undertaken because of our reservations to their experimental design, we concur with their conclusion of an hepatic influence on sodium excretion based on our experiments. Additional experiments presented here, which indicate that a dose-related response occurs with increased portal levels of sodium, provide further evidence for the involvement of the liver in the control of sodium excretion.