Negative feedforward control of body fluid homeostasis by hepatorenal reflex

Abstract

The liver, well known for its role in metabolism, clearance and storage can also be regarded as a sensory organ. The liver is an ideal place to monitor the quality and quantity of absorbed substances, because portal blood delivers substances absorbed from the intestine to the liver and these substances circulate in the hepatic vasculature before substances enter the systemic circulation. Sodium (Na(+))-sensitive mechanism exists in the liver; it is stimulated by the increase in Na(+) concentration in the portal vein, and then hepatorenal reflex is triggered. Renal sympathetic nerve activity is reflexively decreased and urinary Na(+) excretion is increased. This Na(+)-sensitive hepatorenal reflex has a significant role in post-prandial natriuresis. However, the long-term role of this reflex in Na(+) homeostasis may be less important, probably because of the desensitization of Na(+)-sensitive mechanisms. Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) is involved in the hepatoportal Na(+)-sensitive mechanism, and NKCC1 expression is reduced if the hepatoportal region is exposed to high Na(+) concentrations for a long time. This situation occurs when animals intake a high-sodium chloride diet for a long time. Liver cirrhosis also impairs the Na(+)-sensitive hepatorenal reflex. Hepatoportal baroreceptor-induced renal sympathetic excitation and the impaired Na(+)-sensitive hepatorenal reflex may partially explain the Na(+) retention in liver cirrhosis.