| pubmed-article:2831731 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2831731 | lifeskim:mentions | umls-concept:C0439849 | lld:lifeskim |
| pubmed-article:2831731 | lifeskim:mentions | umls-concept:C0521378 | lld:lifeskim |
| pubmed-article:2831731 | lifeskim:mentions | umls-concept:C0042105 | lld:lifeskim |
| pubmed-article:2831731 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:2831731 | lifeskim:mentions | umls-concept:C0678640 | lld:lifeskim |
| pubmed-article:2831731 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
| pubmed-article:2831731 | lifeskim:mentions | umls-concept:C0243077 | lld:lifeskim |
| pubmed-article:2831731 | pubmed:issue | 2 Pt 1 | lld:pubmed |
| pubmed-article:2831731 | pubmed:dateCreated | 1988-4-11 | lld:pubmed |
| pubmed-article:2831731 | pubmed:abstractText | We have recently shown that substitution of Li+ for perfusate Na+ eliminates the HCO3(-)-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+-H+ exchange in the choleresis produced by these bile acids, both Li+ substitution and amiloride affect other cellular processes, including Na+-K+-ATPase activity. We have now further explored both the relationship between UDCA-stimulated bile flow and biliary HCO3- secretion and the possible role of Na+-H+ 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). In the absence of inhibitor, UDCA increased biliary HCO3- concentration ([HCO3-]) up to an apparent maximum of 60-70 mM, and bile flow and biliary HCO3- output appeared to be linearly related over a sixfold range of bile flow rates. Amiloride, DMA, and EIA each produced a concentration-dependent inhibition of UDCA-stimulated bile flow and biliary HCO3- output with an apparent rank order potency (EIA greater than DMA greater than amiloride) similar to that reported for inhibition of Na+-H+ exchange in other systems. None of the inhibitors significantly altered biliary UDCA output or the relationship between UDCA-induced bile flow and either biliary [HCO3-] or biliary HCO3- output. Effects of these inhibitors did not appear attributable either to nonspecific toxicity, as reflected by hepatic release of lactate dehydrogenase or K+, or to inhibition of hepatic Na+-K+-ATPase, measured as Na+-dependent uptake of 86Rb. In contrast to their effects on UDCA choleresis, these inhibitors had little or no effect on basal bile flow, biliary [HCO3-], and biliary HCO3- output. These findings indicate that UDCA-induced but not basal bile formation is closely coupled to biliary HCO3- concentration and output, and they provide additional evidence that UDCA choleresis requires an intact Na+-H+ exchange mechanism. | lld:pubmed |
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| pubmed-article:2831731 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2831731 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2831731 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2831731 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2831731 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:2831731 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:2831731 | pubmed:author | pubmed-author:LakeJ RJR | lld:pubmed |
| pubmed-article:2831731 | pubmed:author | pubmed-author:CragoeE JEJJr | lld:pubmed |
| pubmed-article:2831731 | pubmed:author | pubmed-author:ScharschmidtB... | lld:pubmed |
| pubmed-article:2831731 | pubmed:author | pubmed-author:Van DykeR WRW | lld:pubmed |
| pubmed-article:2831731 | pubmed:author | pubmed-author:RennerE LEL | lld:pubmed |
| pubmed-article:2831731 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2831731 | pubmed:volume | 254 | lld:pubmed |
| pubmed-article:2831731 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2831731 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2831731 | pubmed:pagination | G232-41 | lld:pubmed |
| pubmed-article:2831731 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:2831731 | pubmed:meshHeading | pubmed-meshheading:2831731-... | lld:pubmed |
| pubmed-article:2831731 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:2831731 | pubmed:articleTitle | Ursodeoxycholic acid choleresis: relationship to biliary HCO-3 and effects of Na+-H+ exchange inhibitors. | lld:pubmed |
| pubmed-article:2831731 | pubmed:affiliation | Department of Medicine, University of California School of Medicine, San Francisco 94143. | lld:pubmed |
| pubmed-article:2831731 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2831731 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2831731 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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