The effect of amiloride on biliary HCO‐3‐secretion in the anaesthetized pig.Acta Physiol Scand130, 447–455. Received 20 October 1986, accepted 23 February 1987. ISSN 0001–6772. Institute for Experimental Medical Research, University of Oslo and Surgical Department, Ullevaal Hospital, Oslo, Norway. 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 HCO‐3compared with taurocholic acid (TCA). The slope relating biliary HCO‐3secretion 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 HCO‐3secretion. 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 HCO‐3secretion would be translated into an equimolar fall in biliary HCO‐3secretion. We found that amiloride (2.0 ± 10‐‐4mol l‐1plasma) reduced UDCA‐dependent canalicular HCO‐3secretion by 26 (14–35)% without concurrently reducing bile acid secretion. Amiloride (2.9 ± 10‐‐4mol 1‐‐1plasma) did not significantly reduce secretin‐dependent ductular HCO‐3secretion. 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 HCO‐3secretion, but not for secretin‐dependent ductular HCO‐3secretion.
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Grotmol et al. (1987) studied this question.
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