Ursodeoxycholic acid and certain other bile acids induce a 'hyper' choleresis in several species, including man, which results mainly from active secretion of HCO 3 -.

In theory, one bile acid molecule could recycle several times, thereby generating several HCO 3 -ions in the canaliculus, and this would explain the 'hyper' choleresis.

This HCO 3 -rich choleresis may partly explain the apparently beneficial effects of ursodeoxycholic acid in cholestatic liver diseases, and also its tendency to induce surface gall stone calcification, one of the factors limiting its efficacy as a cholesterol gall stone dissolving agent.

The HCO 3 -rich 'hyper' choleresis induced by ursodeoxycholic acid is partly inhibited by amiloride and by Na + removal, suggesting that the hepatocyte basolateral Na + /H + exchanger contributes to this H + extrusion.