Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2 Pt 1
|
pubmed:dateCreated |
1991-9-19
|
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.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Amphotericin B,
http://linkedlifedata.com/resource/pubmed/chemical/Bumetanide,
http://linkedlifedata.com/resource/pubmed/chemical/Ouabain,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0002-9513
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
261
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
C332-41
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:1872375-Adolescent,
pubmed-meshheading:1872375-Adult,
pubmed-meshheading:1872375-Amiloride,
pubmed-meshheading:1872375-Amphotericin B,
pubmed-meshheading:1872375-Biological Transport,
pubmed-meshheading:1872375-Bumetanide,
pubmed-meshheading:1872375-Cells, Cultured,
pubmed-meshheading:1872375-Child,
pubmed-meshheading:1872375-Cystic Fibrosis,
pubmed-meshheading:1872375-Electrophysiology,
pubmed-meshheading:1872375-Epithelium,
pubmed-meshheading:1872375-Female,
pubmed-meshheading:1872375-Humans,
pubmed-meshheading:1872375-Male,
pubmed-meshheading:1872375-Nasal Mucosa,
pubmed-meshheading:1872375-Osmolar Concentration,
pubmed-meshheading:1872375-Ouabain,
pubmed-meshheading:1872375-Sodium
|
pubmed:year |
1991
|
pubmed:articleTitle |
Transcellular sodium transport in cultured cystic fibrosis human nasal epithelium.
|
pubmed:affiliation |
Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill 27514.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|