Circulating bile is the main factor responsible for atrial natriuretic peptide release in experimental obstructive jaundice.

Abstract

Biliary obstruction in the rabbit causes increased release of atrial natriuretic peptide (ANP). Circulating bile, raised biliary pressure or absence of bile in the duodenum may be implicated in this hepatocardiac syndrome. An experimental model was developed to elucidate the mechanism linking obstructive jaundice and increased plasma ANP. Hepatic and renal function, biliary tree pressure and ANP plasma concentrations were investigated in conscious rabbits 4 and 24 h after common bile duct ligation, biliovenous shunting or external drainage via a biliary fistula. Bilirubin concentration increased after bile duct ligation and creation of a biliovenous shunt. Plasma creatinine increased abruptly in rabbits with a biliovenous shunt. At 4 h, the ANP increase in animals with a biliovenous shunt was ninefold that observed after bile duct obstruction while no change was noted after external biliary diversion (mean 350 versus 45 versus 9 fmol/l; P < 0.01). Relief of biliary tree obstruction was associated with a return of ANP levels towards basal normal values. Raised plasma ANP in obstructive jaundice is not the result of an increased biliary pressure per se or absence of bile in the proximal duodenum but of the passage of bile components to the circulation.