pubmed-article:17978813 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17978813 | lifeskim:mentions | umls-concept:C0012177 | lld:lifeskim |
pubmed-article:17978813 | lifeskim:mentions | umls-concept:C0022646 | lld:lifeskim |
pubmed-article:17978813 | lifeskim:mentions | umls-concept:C0017654 | lld:lifeskim |
pubmed-article:17978813 | lifeskim:mentions | umls-concept:C0015127 | lld:lifeskim |
pubmed-article:17978813 | lifeskim:mentions | umls-concept:C0059285 | lld:lifeskim |
pubmed-article:17978813 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
pubmed-article:17978813 | lifeskim:mentions | umls-concept:C0220981 | lld:lifeskim |
pubmed-article:17978813 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
pubmed-article:17978813 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:17978813 | pubmed:dateCreated | 2007-12-31 | lld:pubmed |
pubmed-article:17978813 | pubmed:abstractText | Dietary casein promotes a progressive decline in the glomerular filtration rate (GFR) of remnant kidneys associated with metabolic acidosis and an endothelin-mediated increase in renal acidification. We tested whether diets that affect the acid-base status contributes to the decline of GFR through endothelin receptors in rats with a remnant kidney. Rats on a casein diet had metabolic acidosis at baseline and developed a progressive decline in GFR after renal mass reduction. Dietary sodium bicarbonate but not sodium chloride ameliorated metabolic acidosis and prevented the decrease in GFR but only after the sodium bicarbonate-induced increase in blood pressure was treated. Dietary soy protein did not induce baseline metabolic acidosis and rats with remnant kidney on a soy diet had no decrease in their GFR. By contrast, rats with a remnant kidney on soy protein given dietary acid developed metabolic acidosis and a decreased GFR. This decline in GFR was prevented in either case by endothelin A but not endothelin A/B receptor antagonism. Our study suggests that the casein-induced decline in GFR of the remnant kidney is mediated by metabolic acidosis through endothelin A receptors. | lld:pubmed |
pubmed-article:17978813 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17978813 | pubmed:language | eng | lld:pubmed |
pubmed-article:17978813 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17978813 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17978813 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17978813 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17978813 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17978813 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17978813 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17978813 | pubmed:month | Jan | lld:pubmed |
pubmed-article:17978813 | pubmed:issn | 0085-2538 | lld:pubmed |
pubmed-article:17978813 | pubmed:author | pubmed-author:SimoniJJ | lld:pubmed |
pubmed-article:17978813 | pubmed:author | pubmed-author:HackerCC | lld:pubmed |
pubmed-article:17978813 | pubmed:author | pubmed-author:WessonD EDE | lld:pubmed |
pubmed-article:17978813 | pubmed:author | pubmed-author:TranR MRM | lld:pubmed |
pubmed-article:17978813 | pubmed:author | pubmed-author:PhisitkulSS | lld:pubmed |
pubmed-article:17978813 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17978813 | pubmed:volume | 73 | lld:pubmed |
pubmed-article:17978813 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17978813 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17978813 | pubmed:pagination | 192-9 | lld:pubmed |
pubmed-article:17978813 | pubmed:dateRevised | 2009-2-9 | lld:pubmed |
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pubmed-article:17978813 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:17978813 | pubmed:articleTitle | Dietary protein causes a decline in the glomerular filtration rate of the remnant kidney mediated by metabolic acidosis and endothelin receptors. | lld:pubmed |
pubmed-article:17978813 | pubmed:affiliation | Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA. | lld:pubmed |
pubmed-article:17978813 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17978813 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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