Steroid hormone-dependent expression of blocker-sensitive ENaCs in apical membranes of A6 epithelia

Lynn M. Baxendale-Cox, Randall L. Duncan, Xuehong Liu, Kieron Baldwin, Willem J. Els, Sandy I. Helman

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Weak channel blocker-induced noise analysis was used to determine the way in which the steroids aldosterone and corticosterone stimulated apical membrane Na+ entry into the cells of tissue-cultured A6 epithelia. Among groups of tissues grown on a variety of substrates, in a variety of growth media, and with cells at passages 73-112, the steroids stimulated both amiloride-sensitive and amiloride-insensitive Na+ transport as measured by short-circuit currents in chambers perfused with either growth medium or a Ringer solution. From baseline rates of blocker-sensitive short-circuit current between 2 and 7 μA/cm2, transport was stimulated about threefold in all groups of experiments. Single channel currents averaged near 0.3 pA (growth medium) and 0.5 pA (Ringer) and were decreased 6-20% from controls by steroid due to the expected decreases of fractional transcellular resistance. Irrespective of baseline transport rates, the steroids in all groups of tissues stimulated transport by increase of the density of blocker-sensitive epithelial Na+ channels (ENaCs). Channel open probability was the same in control and stimulated tissues, averaging ~0.3 in all groups of tissues. Accordingly, steroid-mediated increases of open channel density responsible for stimulation of Na+ transport are due to increases of the apical membrane pool of functional channels and not their open probability.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume273
Issue number5 42-5
StatePublished - 1997
Externally publishedYes

Fingerprint

Steroid hormones
Epithelial Sodium Channels
Epithelium
Steroids
Hormones
Tissue
Membranes
Amiloride
Short circuit currents
Growth
Corticosterone
Aldosterone
Noise
Cultured Cells
Substrates
Experiments

Keywords

  • Cortical collecting ducts
  • Electrophysiology
  • Kidney
  • Noise analysis
  • Sodium channels
  • Tissue culture

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology
  • Physiology (medical)

Cite this

Baxendale-Cox, L. M., Duncan, R. L., Liu, X., Baldwin, K., Els, W. J., & Helman, S. I. (1997). Steroid hormone-dependent expression of blocker-sensitive ENaCs in apical membranes of A6 epithelia. American Journal of Physiology - Cell Physiology, 273(5 42-5).

Steroid hormone-dependent expression of blocker-sensitive ENaCs in apical membranes of A6 epithelia. / Baxendale-Cox, Lynn M.; Duncan, Randall L.; Liu, Xuehong; Baldwin, Kieron; Els, Willem J.; Helman, Sandy I.

In: American Journal of Physiology - Cell Physiology, Vol. 273, No. 5 42-5, 1997.

Research output: Contribution to journalArticle

Baxendale-Cox, LM, Duncan, RL, Liu, X, Baldwin, K, Els, WJ & Helman, SI 1997, 'Steroid hormone-dependent expression of blocker-sensitive ENaCs in apical membranes of A6 epithelia', American Journal of Physiology - Cell Physiology, vol. 273, no. 5 42-5.
Baxendale-Cox, Lynn M. ; Duncan, Randall L. ; Liu, Xuehong ; Baldwin, Kieron ; Els, Willem J. ; Helman, Sandy I. / Steroid hormone-dependent expression of blocker-sensitive ENaCs in apical membranes of A6 epithelia. In: American Journal of Physiology - Cell Physiology. 1997 ; Vol. 273, No. 5 42-5.
@article{69a2f5caecdb44f9b629efff1793e7d9,
title = "Steroid hormone-dependent expression of blocker-sensitive ENaCs in apical membranes of A6 epithelia",
abstract = "Weak channel blocker-induced noise analysis was used to determine the way in which the steroids aldosterone and corticosterone stimulated apical membrane Na+ entry into the cells of tissue-cultured A6 epithelia. Among groups of tissues grown on a variety of substrates, in a variety of growth media, and with cells at passages 73-112, the steroids stimulated both amiloride-sensitive and amiloride-insensitive Na+ transport as measured by short-circuit currents in chambers perfused with either growth medium or a Ringer solution. From baseline rates of blocker-sensitive short-circuit current between 2 and 7 μA/cm2, transport was stimulated about threefold in all groups of experiments. Single channel currents averaged near 0.3 pA (growth medium) and 0.5 pA (Ringer) and were decreased 6-20{\%} from controls by steroid due to the expected decreases of fractional transcellular resistance. Irrespective of baseline transport rates, the steroids in all groups of tissues stimulated transport by increase of the density of blocker-sensitive epithelial Na+ channels (ENaCs). Channel open probability was the same in control and stimulated tissues, averaging ~0.3 in all groups of tissues. Accordingly, steroid-mediated increases of open channel density responsible for stimulation of Na+ transport are due to increases of the apical membrane pool of functional channels and not their open probability.",
keywords = "Cortical collecting ducts, Electrophysiology, Kidney, Noise analysis, Sodium channels, Tissue culture",
author = "Baxendale-Cox, {Lynn M.} and Duncan, {Randall L.} and Xuehong Liu and Kieron Baldwin and Els, {Willem J.} and Helman, {Sandy I.}",
year = "1997",
language = "English (US)",
volume = "273",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "5 42-5",

}

TY - JOUR

T1 - Steroid hormone-dependent expression of blocker-sensitive ENaCs in apical membranes of A6 epithelia

AU - Baxendale-Cox, Lynn M.

AU - Duncan, Randall L.

AU - Liu, Xuehong

AU - Baldwin, Kieron

AU - Els, Willem J.

AU - Helman, Sandy I.

PY - 1997

Y1 - 1997

N2 - Weak channel blocker-induced noise analysis was used to determine the way in which the steroids aldosterone and corticosterone stimulated apical membrane Na+ entry into the cells of tissue-cultured A6 epithelia. Among groups of tissues grown on a variety of substrates, in a variety of growth media, and with cells at passages 73-112, the steroids stimulated both amiloride-sensitive and amiloride-insensitive Na+ transport as measured by short-circuit currents in chambers perfused with either growth medium or a Ringer solution. From baseline rates of blocker-sensitive short-circuit current between 2 and 7 μA/cm2, transport was stimulated about threefold in all groups of experiments. Single channel currents averaged near 0.3 pA (growth medium) and 0.5 pA (Ringer) and were decreased 6-20% from controls by steroid due to the expected decreases of fractional transcellular resistance. Irrespective of baseline transport rates, the steroids in all groups of tissues stimulated transport by increase of the density of blocker-sensitive epithelial Na+ channels (ENaCs). Channel open probability was the same in control and stimulated tissues, averaging ~0.3 in all groups of tissues. Accordingly, steroid-mediated increases of open channel density responsible for stimulation of Na+ transport are due to increases of the apical membrane pool of functional channels and not their open probability.

AB - Weak channel blocker-induced noise analysis was used to determine the way in which the steroids aldosterone and corticosterone stimulated apical membrane Na+ entry into the cells of tissue-cultured A6 epithelia. Among groups of tissues grown on a variety of substrates, in a variety of growth media, and with cells at passages 73-112, the steroids stimulated both amiloride-sensitive and amiloride-insensitive Na+ transport as measured by short-circuit currents in chambers perfused with either growth medium or a Ringer solution. From baseline rates of blocker-sensitive short-circuit current between 2 and 7 μA/cm2, transport was stimulated about threefold in all groups of experiments. Single channel currents averaged near 0.3 pA (growth medium) and 0.5 pA (Ringer) and were decreased 6-20% from controls by steroid due to the expected decreases of fractional transcellular resistance. Irrespective of baseline transport rates, the steroids in all groups of tissues stimulated transport by increase of the density of blocker-sensitive epithelial Na+ channels (ENaCs). Channel open probability was the same in control and stimulated tissues, averaging ~0.3 in all groups of tissues. Accordingly, steroid-mediated increases of open channel density responsible for stimulation of Na+ transport are due to increases of the apical membrane pool of functional channels and not their open probability.

KW - Cortical collecting ducts

KW - Electrophysiology

KW - Kidney

KW - Noise analysis

KW - Sodium channels

KW - Tissue culture

UR - http://www.scopus.com/inward/record.url?scp=0030699418&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030699418&partnerID=8YFLogxK

M3 - Article

VL - 273

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 5 42-5

ER -