pubmed-article:1872375 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1872375 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:1872375 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
pubmed-article:1872375 | lifeskim:mentions | umls-concept:C0010674 | lld:lifeskim |
pubmed-article:1872375 | lifeskim:mentions | umls-concept:C0599331 | lld:lifeskim |
pubmed-article:1872375 | lifeskim:mentions | umls-concept:C1159690 | lld:lifeskim |
pubmed-article:1872375 | pubmed:issue | 2 Pt 1 | lld:pubmed |
pubmed-article:1872375 | pubmed:dateCreated | 1991-9-19 | lld:pubmed |
pubmed-article:1872375 | pubmed:abstractText | Cystic fibrosis (CF) airway epithelia exhibit raised transepithelial Na+ transport rates, as determined by open-circuit isotope fluxes and estimates of the amiloride-sensitive equivalent short-circuit current (Ieq). To study the contribution of apical and basolateral membrane paths to raised Na+ transport in CF, CF nasal epithelial cultures were studied with double-barreled Na(+)-selective microelectrodes and the Ussing chamber technique. Intracellular Na+ activity (acNa) was 24.1 +/- 1.5 mM (n = 36), a value similar to acNa of normal nasal epithelial cells. Reduction of luminal [Na+] to 3 mM abolished Ieq and reduced acNa. Amiloride (10(-4) M) abolished Ieq but increased acNa from 20 +/- 2 to 36 +/- 7 mM (n = 10). Amiloride-induced increase in acNa was not affected by serosal [Na+] reduction but was blocked by preexposure to reduced luminal [Na+]. Amphotericin B increased Ieq during amiloride exposure, indicating that amiloride did not inhibit NA(+)-K(+)-ATPase. Ouabain abolished Ieq and slowly raised acNa. Reduction of serosal [Na+] led to a decrease in acNa that was blocked by bumetanide. It is concluded that 1) CF airway epithelia exhibit an increased apical membrane Na+ permeability, 2) acNa is regulated to a normal level in CF cells despite increased transcellular Na+ fluxes, 3) the abnormal increase in acNa in response to amiloride is dependent on luminal Na+, 4) Na+ is transported across the basolateral membrane by a bumetanide-sensitive cotransport mechanism, and 5) ouabain inhibits the basolateral Na(+)-K(+)-ATPase, causing slow dissipation of the chemical and electrical gradients across the cell membranes. | lld:pubmed |
pubmed-article:1872375 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1872375 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1872375 | pubmed:language | eng | lld:pubmed |
pubmed-article:1872375 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1872375 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1872375 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1872375 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1872375 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1872375 | pubmed:month | Aug | lld:pubmed |
pubmed-article:1872375 | pubmed:issn | 0002-9513 | lld:pubmed |
pubmed-article:1872375 | pubmed:author | pubmed-author:BoucherR CRC | lld:pubmed |
pubmed-article:1872375 | pubmed:author | pubmed-author:WillumsenN... | lld:pubmed |
pubmed-article:1872375 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1872375 | pubmed:volume | 261 | lld:pubmed |
pubmed-article:1872375 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1872375 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1872375 | pubmed:pagination | C332-41 | lld:pubmed |
pubmed-article:1872375 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:1872375 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1872375 | pubmed:articleTitle | Transcellular sodium transport in cultured cystic fibrosis human nasal epithelium. | lld:pubmed |
pubmed-article:1872375 | pubmed:affiliation | Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill 27514. | lld:pubmed |
pubmed-article:1872375 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1872375 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:1872375 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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