Insulin stimulated Na" transport is mediated by increase of apical Na' channels and not open probability in control and aldosterone prestimulated A6 EP1thelia

Bonnie Blazer-Yost, Xuehong Liu, Sandy Helman

Research output: Contribution to journalArticle

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Abstract

Insulin-sensitive A6 epithelia grown on Transwell tissue-culture treated inserts were studied using a non-invasive Na' channel blocker pulse inhibition method II-'ASEB J. 9:A64,1995) to determine apical membrane single channel current (iNa), channel density (Nr) and open probability (PJ. 2.7 uM aldosterone (N=6) increased amiloride-sensitive short-circuit currents (INa) from 1.51±0.26 (N=5) to 6.20±0.42 liA/cm' due to increase of Nr (I7.6±4.1 to 57.9±7.2 million channels/cm-', respectively). 20 nM insulin caused maximal increases of Na1 transport within 30 min (control, 264%) and 10 min (aldosterone, 198%). In both control and aldosterone stimulated tissues, the increase of Na" transport was due to increase of N, (49.8±10.1 and 168.9± 19.4 million channels/cm', respectively). iNa was decreased slightly ( 10-20%) from control values averaging near 0.38 pA due to expected changes of fractional transcellular resistance. P remained unchanged in control tissues (0.27±0.01) but was decreased in aldosterone stimulated tissues (0.320.02 to 0.23±0.01). We conclude that both insulin and aldosterone stimulate Na transport by increase of NT. However, the mechanisms are separate and distinct.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number3
StatePublished - 1996
Externally publishedYes

Fingerprint

aldosterone
Aldosterone
insulin
Insulin
Tissue
Tissue culture
Amiloride
Ion Channels
Short circuit currents
tissue culture
epithelium
Epithelium
Membranes
tissues

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Insulin stimulated Na" transport is mediated by increase of apical Na' channels and not open probability in control and aldosterone prestimulated A6 EP1thelia. / Blazer-Yost, Bonnie; Liu, Xuehong; Helman, Sandy.

In: FASEB Journal, Vol. 10, No. 3, 1996.

Research output: Contribution to journalArticle

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abstract = "Insulin-sensitive A6 epithelia grown on Transwell tissue-culture treated inserts were studied using a non-invasive Na' channel blocker pulse inhibition method II-'ASEB J. 9:A64,1995) to determine apical membrane single channel current (iNa), channel density (Nr) and open probability (PJ. 2.7 uM aldosterone (N=6) increased amiloride-sensitive short-circuit currents (INa) from 1.51±0.26 (N=5) to 6.20±0.42 liA/cm' due to increase of Nr (I7.6±4.1 to 57.9±7.2 million channels/cm-', respectively). 20 nM insulin caused maximal increases of Na1 transport within 30 min (control, 264{\%}) and 10 min (aldosterone, 198{\%}). In both control and aldosterone stimulated tissues, the increase of Na{"} transport was due to increase of N, (49.8±10.1 and 168.9± 19.4 million channels/cm', respectively). iNa was decreased slightly ( 10-20{\%}) from control values averaging near 0.38 pA due to expected changes of fractional transcellular resistance. P remained unchanged in control tissues (0.27±0.01) but was decreased in aldosterone stimulated tissues (0.320.02 to 0.23±0.01). We conclude that both insulin and aldosterone stimulate Na transport by increase of NT. However, the mechanisms are separate and distinct.",
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AU - Liu, Xuehong

AU - Helman, Sandy

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