Grotmol T, Buanes T, Raeder M G
Acta Physiol Scand. 1987 Jul;130(3):447-55. doi: 10.1111/j.1748-1716.1987.tb08161.x.
The present study was performed on 29 anaesthetized pigs and shows that the bile acid ursodeoxycholic acid (UDCA) produces a flow of bile rich in HCO3- compared with taurocholic acid (TCA). The slope relating biliary HCO3- secretion to bile acid secretion was 0.59 (0.44-0.82) and 0.33 (0.29-0.38) during venous infusion of UDCA and TCA, respectively. We next wanted to evaluate the importance of Na+/H+ ion exchange for biliary HCO3- secretion. High doses of amiloride were employed in order to impair the hepatic Na+/H+ ion exchanger. It was reasoned that any reduction in H+ efflux through the hepatic Na+/H+ ion exchanger involved in causing biliary HCO3- secretion would be translated into an equimolar fall in biliary HCO3- secretion. We found that amiloride (2.0 X 10(-4) mol l-1 plasma) reduced UDCA-dependent canalicular HCO3- secretion by 26 (14-35)% without concurrently reducing bile acid secretion. Amiloride (2.9 X 10(-4) mol l-1 plasma) did not significantly reduce secretin-dependent ductular HCO3- secretion. In this group of animals amiloride reduced bile acid secretion by 13 (5-22)%. It is concluded that Na+/H+ ion exchanger is essential for UDCA-dependent canalicular HCO3- secretion, but not for secretin-dependent ductular HCO3- secretion.
