Source:http://linkedlifedata.com/resource/pubmed/id/17507603
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2007-8-31
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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.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Captopril,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Drug,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Chloride Symporters,
http://linkedlifedata.com/resource/pubmed/chemical/thiazide receptor
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1931-857X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
293
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
F662-9
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pubmed:dateRevised |
2011-4-28
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pubmed:meshHeading |
pubmed-meshheading:17507603-Angiotensin II,
pubmed-meshheading:17507603-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:17507603-Animals,
pubmed-meshheading:17507603-Captopril,
pubmed-meshheading:17507603-Gene Expression Regulation,
pubmed-meshheading:17507603-Kidney Tubules, Distal,
pubmed-meshheading:17507603-Microscopy, Immunoelectron,
pubmed-meshheading:17507603-Protein Transport,
pubmed-meshheading:17507603-Rats,
pubmed-meshheading:17507603-Rats, Sprague-Dawley,
pubmed-meshheading:17507603-Receptors, Drug,
pubmed-meshheading:17507603-Sodium Chloride Symporters
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pubmed:year |
2007
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pubmed:articleTitle |
ANG II provokes acute trafficking of distal tubule Na+-Cl(-) cotransporter to apical membrane.
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pubmed:affiliation |
Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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