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| pubmed-article:15849232 | lifeskim:mentions | umls-concept:C0003765 | lld:lifeskim |
| pubmed-article:15849232 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:15849232 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:15849232 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:15849232 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:15849232 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:15849232 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:15849232 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:15849232 | pubmed:dateCreated | 2005-9-15 | lld:pubmed |
| pubmed-article:15849232 | pubmed:abstractText | In cultured endothelial cells, 70-95% of extracellular l-arginine uptake has been attributed to the cationic amino acid transporter-1 protein (CAT-1). We tested the hypothesis that extracellular l-arginine entry into endothelial cells via CAT-1 plays a crucial role in endothelial nitric oxide (NO) production during in vivo conditions. Using l-lysine, the preferred amino acid transported by CAT-1, we competitively inhibited extracellular l-arginine transport into endothelial cells during conditions of NaCl hyperosmolarity, low oxygen, and flow increase. Our prior studies indicate that each of these perturbations causes NO-dependent vasodilation. The perivascular NO concentration ([NO]) and blood flow were determined in the in vivo rat intestinal microvasculature. Suppression of extracellular l-arginine transport significantly and strongly inhibited increases in vascular [NO] and intestinal blood flow during NaCl hyperosmolarity, lowered oxygen tension, and increased flow. These results suggest that l-arginine from the extracellular space is accumulated by CAT-1. When CAT-1-mediated transport of extracellular l-arginine into endothelial cells was suppressed, the endothelial cell NO response to a wide range of physiological stimuli was strongly depressed. | lld:pubmed |
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| pubmed-article:15849232 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15849232 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15849232 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15849232 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15849232 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:15849232 | pubmed:issn | 0363-6135 | lld:pubmed |
| pubmed-article:15849232 | pubmed:author | pubmed-author:BohlenH... | lld:pubmed |
| pubmed-article:15849232 | pubmed:author | pubmed-author:ZaniBrett GBG | lld:pubmed |
| pubmed-article:15849232 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15849232 | pubmed:volume | 289 | lld:pubmed |
| pubmed-article:15849232 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15849232 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15849232 | pubmed:pagination | H1381-90 | lld:pubmed |
| pubmed-article:15849232 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15849232 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15849232 | pubmed:articleTitle | Transport of extracellular l-arginine via cationic amino acid transporter is required during in vivo endothelial nitric oxide production. | lld:pubmed |
| pubmed-article:15849232 | pubmed:affiliation | Department of Cellular and Integrative Physiology, Indiana University Medical School, 635 Barnhill Drive, Indianapolis, IN 46202, USA. | lld:pubmed |
| pubmed-article:15849232 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15849232 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15849232 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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