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

5 Scopus citations

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)
Pages (from-to)A78
JournalFASEB Journal
Volume10
Issue number3
StatePublished - Dec 1 1996

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Fingerprint Dive into the research topics of 'Insulin stimulated Na" transport is mediated by increase of apical Na' channels and not open probability in control and aldosterone prestimulated A6 EP1thelia'. Together they form a unique fingerprint.

  • Cite this