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- W213749513 abstract "The authors have recently shown that substitution of Li{sup +} for perfusate Na{sup +} eliminates the HCO{sub 3}{sup {minus}}-rich choleresis produced by ursodeoxycholic acid (UDCA) in isolated perfused rat liver and that the increase in bile flow produced by both UDCA and taurocholic acid is partially inhibited by 1 mM amiloride. Although these findings are consistent with a role for Na{sup +}-H{sup +} exchange in the choleresis produced by these bile acids, both Li{sup +} substitution and amiloride affect other cellular processes, including Na{sup +}-K{sup +}-ATPase activity. They have now further explored both the relationship between UDCA-stimulated bile flow and biliary HCO{sub 3}{sup {minus}} secretion and the possible role of Na{sup +}-H{sup +} exchange in this process by comparing the effects of amiloride with two of its more potent and presumably more specific analogues, 5-(N,N-dimethyl)amiloride hydrochloride (DMA) and 5-(N-ethyl-N-isopropyl)amiloride (EIA). None of the inhibitors significantly altered biliary UDCA output or the relationship between UDCA-induced bile flow and either biliary (HCO{sub 3}{sup {minus}}) or biliary HCO{sub 3}{sub {minus}} output. Effects of these inhibitors did not appear attributable either to nonspecific toxicity, as reflected by hepatic release of lactate dehydrogenase or K{sup +}, or to inhibition of hepatic Na{sup +}-K{sup +}-ATPase, measuredmore » as Na{sup +}-dependent uptake of {sup 86}Rb. These findings indicate that UDCA-induced but not basal bile formation is closely coupled to biliary HCO{sub 3}{sup {minus}} concentration and output, and they provide additional evidence that UDCA choleresis requires an intact Na{sup +}-H{sup +} exchange mechanism.« less" @default.
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- W213749513 date "1988-02-01" @default.
- W213749513 modified "2023-09-26" @default.
- W213749513 title "Ursodeoxycholic acid choleresis: Relationship to biliary HCO sup minus sub 3 and effects of Na sup + -H sup + exchange inhibitors" @default.
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