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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5 Pt 2
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pubmed:dateCreated |
1995-7-6
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pubmed:abstractText |
The furosemide sensitivity of the tubuloglomerular feedback (TGF) response has suggested an important role for the Na-2Cl-K cotransporter in the mechanism by which increased luminal NaCl concentration causes afferent arteriolar vasoconstriction. The present experiments in anesthetized rats were performed to evaluate the effect of K channel blockade with Ba on TGF, since Ba has been shown to inhibit NaCl transport in the thick ascending limb. The presence of either 1.5 or 2 mM BaCl2 during retrograde perfusion with a 135 mM NaCl solution reduced the decrease of early proximal flow rate (VEP) by 2.7 +/- 0.76 (P < 0.02) and 4.2 +/- 0.8 nl/min (P < 0.01) compared with perfusion without BaCl2. Retrograde perfusion with 38 mM NaCl + 5 mM KCl reduced VEP by 10.4 +/- 1.3 nl/min, whereas 40 mM NaCl + 1.5 mM BaCl2 caused a reduction by only 6.1 +/- 1.4 nl/min (P < 0.001). In contrast to the inhibition caused by retrograde perfusion with low concentrations of BaCl2, increased vasoconstriction was seen during retrograde perfusion with 5 mM BaCl2 or during orthograde perfusion with 10 mM BaCl2. The addition of 10(-4) M furosemide to a solution containing 5 mM BaCl2 largely blocked the increased vasoconstrictor response. Peritubular perfusion with a solution containing 5 mM BaCl2 caused a fall in stop-flow pressure in an adjacent nephron by 10.7 +/- 1.5 mmHg (P < 0.001). These results indicate that under our experimental conditions Ba ions exert a dual effect on vascular responses to changes in luminal NaCl concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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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/Barium,
http://linkedlifedata.com/resource/pubmed/chemical/Furosemide,
http://linkedlifedata.com/resource/pubmed/chemical/Ions,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
268
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
F960-6
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7771525-Animals,
pubmed-meshheading:7771525-Barium,
pubmed-meshheading:7771525-Feedback,
pubmed-meshheading:7771525-Furosemide,
pubmed-meshheading:7771525-Ions,
pubmed-meshheading:7771525-Kidney Glomerulus,
pubmed-meshheading:7771525-Kidney Tubules,
pubmed-meshheading:7771525-Male,
pubmed-meshheading:7771525-Osmolar Concentration,
pubmed-meshheading:7771525-Perfusion,
pubmed-meshheading:7771525-Potassium Channel Blockers,
pubmed-meshheading:7771525-Rats,
pubmed-meshheading:7771525-Rats, Sprague-Dawley,
pubmed-meshheading:7771525-Transforming Growth Factors
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pubmed:year |
1995
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pubmed:articleTitle |
Effects of barium ions on tubuloglomerular feedback.
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pubmed:affiliation |
Department of Physiology, University of Michigan, Ann Arbor 48104, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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