| pubmed-article:14732722 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14732722 | lifeskim:mentions | umls-concept:C0020538 | lld:lifeskim |
| pubmed-article:14732722 | lifeskim:mentions | umls-concept:C0022646 | lld:lifeskim |
| pubmed-article:14732722 | lifeskim:mentions | umls-concept:C0033551 | lld:lifeskim |
| pubmed-article:14732722 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:14732722 | pubmed:dateCreated | 2004-2-27 | lld:pubmed |
| pubmed-article:14732722 | pubmed:abstractText | Selective cyclooxygenase (COX)-2 inhibitors that are in widespread clinical use were developed to avoid side effects of conventional NSAIDs, including gastrointestinal and renal toxicity. However, COX-2 is constitutively expressed in the kidney and is highly regulated in response to alterations in intravascular volume. COX-2 metabolites have been implicated in maintenance of renal blood flow, mediation of renin release, and regulation of sodium excretion. COX-2 inhibition may transiently decrease urine sodium excretion in some subjects and induce mild to moderate elevation of blood pressure. Furthermore, in conditions of relative intravascular volume depletion and/or renal hypoperfusion, interference with COX-2 activity can have deleterious effects on maintenance of renal blood flow and glomerular filtration rate. In addition to physiological regulation of COX-2 expression in the kidney, increased renal cortical COX-2 expression is seen in experimental models associated with altered renal hemodynamics and progressive renal injury (decreased renal mass, poorly controlled diabetes), and long-term treatment with selective COX-2 inhibitors ameliorates functional and structural renal damage in these conditions. | lld:pubmed |
| pubmed-article:14732722 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14732722 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14732722 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14732722 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14732722 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14732722 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14732722 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14732722 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14732722 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14732722 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14732722 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:14732722 | pubmed:issn | 1524-4563 | lld:pubmed |
| pubmed-article:14732722 | pubmed:author | pubmed-author:HarrisRaymond... | lld:pubmed |
| pubmed-article:14732722 | pubmed:author | pubmed-author:ChengHui-Fang... | lld:pubmed |
| pubmed-article:14732722 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:14732722 | pubmed:volume | 43 | lld:pubmed |
| pubmed-article:14732722 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14732722 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14732722 | pubmed:pagination | 525-30 | lld:pubmed |
| pubmed-article:14732722 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
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| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
| pubmed-article:14732722 | pubmed:meshHeading | pubmed-meshheading:14732722... | lld:pubmed |
| pubmed-article:14732722 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:14732722 | pubmed:articleTitle | Cyclooxygenases, the kidney, and hypertension. | lld:pubmed |
| pubmed-article:14732722 | pubmed:affiliation | Division of Nephrology, S 3322 MCN, Vanderbilt University School of Medicine, Nashville, TN 37232-2372, USA. | lld:pubmed |
| pubmed-article:14732722 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14732722 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:14732722 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:14732722 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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