pubmed-article:17507603 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17507603 | lifeskim:mentions | umls-concept:C0205108 | lld:lifeskim |
pubmed-article:17507603 | lifeskim:mentions | umls-concept:C0596119 | lld:lifeskim |
pubmed-article:17507603 | lifeskim:mentions | umls-concept:C0205178 | lld:lifeskim |
pubmed-article:17507603 | lifeskim:mentions | umls-concept:C1367482 | lld:lifeskim |
pubmed-article:17507603 | lifeskim:mentions | umls-concept:C0599896 | lld:lifeskim |
pubmed-article:17507603 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
pubmed-article:17507603 | lifeskim:mentions | umls-concept:C0598850 | lld:lifeskim |
pubmed-article:17507603 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:17507603 | pubmed:dateCreated | 2007-8-31 | lld:pubmed |
pubmed-article:17507603 | pubmed:abstractText | The distal convoluted tubule (DCT) Na+-Cl(-) cotransporter (NCC), the target of thiazide diuretics, is responsible for the reabsorption of 5-10% of filtered NaCl. The aim of this study was to test the hypothesis that acute infusion of the angiotensin-converting enzyme (ACE) inhibitor captopril (at 12 microg/min) for 20 min provokes trafficking of NCC from apical plasma membranes (APM) to subapical cytoplasmic vesicles (SCV), which is reversed by acute ANG II infusion (ANG II at 20 ng.kg(-1).min(-1) along with 12 microg/min captopril) for 20 min in male Sprague-Dawley rats (250-350 g). By immuno-electron microscopy using an anti-NCC (D. Ellison) 71.5 +/- SD 4.9% of the NCC gold labeling was associated with the APM in control, sham operated, and infused rats, while captopril infusion reduced NCC in APM to 54.9 +/- 6.9% (P < 0.001) and markedly increased immunogold labeling of SCV. Subsequent infusion of ANG II with captopril restored NCC immunogold labeling of APM to 72.4 +/- 4.2%, that is, 20% of the total NCC trafficked between APM and SCV. Likewise, on density gradients of cortex, captopril provoked redistribution of 27.3% of total NCC from low-density APM-enriched membranes to higher-density membranes and ANG II+captopril restored 20.3% of the NCC to APM-enriched fractions. Redistribution occurred independent of a change in NCC total abundance. In conclusion, this study demonstrates that ACE inhibition provokes acute trafficking of NCC out of the plasma membrane, which likely decreases DCT Na+ reabsorption, while ANG II provokes rapid trafficking of NCC from stores in subapical vesicles to the plasma membrane, which likely increases DCT Na+ reabsorption. | lld:pubmed |
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pubmed-article:17507603 | pubmed:language | eng | lld:pubmed |
pubmed-article:17507603 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17507603 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17507603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17507603 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17507603 | pubmed:month | Sep | lld:pubmed |
pubmed-article:17507603 | pubmed:issn | 1931-857X | lld:pubmed |
pubmed-article:17507603 | pubmed:author | pubmed-author:McDonoughAlic... | lld:pubmed |
pubmed-article:17507603 | pubmed:author | pubmed-author:MaunsbachArvi... | lld:pubmed |
pubmed-article:17507603 | pubmed:author | pubmed-author:Pihakaski-Mau... | lld:pubmed |
pubmed-article:17507603 | pubmed:author | pubmed-author:SandbergMonic... | lld:pubmed |
pubmed-article:17507603 | pubmed:author | pubmed-author:RiquierAnne... | lld:pubmed |
pubmed-article:17507603 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17507603 | pubmed:volume | 293 | lld:pubmed |
pubmed-article:17507603 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17507603 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17507603 | pubmed:pagination | F662-9 | lld:pubmed |
pubmed-article:17507603 | pubmed:dateRevised | 2011-4-28 | lld:pubmed |
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pubmed-article:17507603 | pubmed:meshHeading | pubmed-meshheading:17507603... | lld:pubmed |
pubmed-article:17507603 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17507603 | pubmed:articleTitle | ANG II provokes acute trafficking of distal tubule Na+-Cl(-) cotransporter to apical membrane. | lld:pubmed |
pubmed-article:17507603 | pubmed:affiliation | Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California, USA. | lld:pubmed |
pubmed-article:17507603 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17507603 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:17507603 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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