Characterisation of volume-activated ion transport across epithelial monolayers of human intestinal T84 cells

G T McEwan, C D Brown, B H Hirst, N L Simmons

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The effects of hypo-osmolarity upon transepithelial ion transport in human intestinal cell layers have been investigated. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a transient stimulation of inward short-circuit current (Isc). This transient stimulation of inward current by hypo-osmotic media was abolished by 100 mumol/l 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS). After prestimulation of inward Isc by vasoactive intestinal peptide (VIP) or by combinations of carbachol and prostaglandin E1, hypo-osmotic exposure of the basal-lateral surfaces resulted in a further transient stimulation of Isc. The stimulation of Isc in these conditions was largely insensitive to DIDS inhibition. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a stimulation of loop-diuretic-insensitive 86Rb efflux across the basal-lateral surfaces. In addition, hypo-osmotic exposure of T84 cells is also associated with an increase in cytosolic Ca2+. It is concluded that the effects of hypo-osmotic exposure of T84 cells on secretory Isc are consistent with the activation of a DIDS-sensitive apical Cl- conductance and a basal-lateral K+ conductance. With prior activation of inward Isc by VIP via a cAMP-activated DIDS-insensitive apical Cl- conductance, augmentation of the secretory current by hypo-osmotic exposure is likely to result primarily from increased basal-lateral K+ current and loop-diuretic-sensitive Cl- uptake.
Original languageEnglish
Pages (from-to)213-20
Number of pages8
JournalPflugers Archiv : European Journal of Physiology
Volume423
Issue number3-4
Publication statusPublished - May 1993

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Ion Transport
Short circuit currents
Sodium Potassium Chloride Symporter Inhibitors
Monolayers
Vasoactive Intestinal Peptide
Ions
Acids
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
Alprostadil
Carbachol
Osmolar Concentration
Chemical activation
Cells

Keywords

  • 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
  • 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid
  • Biological Transport
  • Calcium
  • Carbachol
  • Cells, Cultured
  • Chlorides
  • Electric Conductivity
  • Epithelium
  • Humans
  • Hypotonic Solutions
  • Intestines
  • Ions
  • Kinetics
  • Osmolar Concentration
  • Prostaglandins E
  • Rubidium Radioisotopes
  • Vasoactive Intestinal Peptide

Cite this

Characterisation of volume-activated ion transport across epithelial monolayers of human intestinal T84 cells. / McEwan, G T; Brown, C D; Hirst, B H; Simmons, N L.

In: Pflugers Archiv : European Journal of Physiology, Vol. 423, No. 3-4, 05.1993, p. 213-20.

Research output: Contribution to journalArticle

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abstract = "The effects of hypo-osmolarity upon transepithelial ion transport in human intestinal cell layers have been investigated. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a transient stimulation of inward short-circuit current (Isc). This transient stimulation of inward current by hypo-osmotic media was abolished by 100 mumol/l 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS). After prestimulation of inward Isc by vasoactive intestinal peptide (VIP) or by combinations of carbachol and prostaglandin E1, hypo-osmotic exposure of the basal-lateral surfaces resulted in a further transient stimulation of Isc. The stimulation of Isc in these conditions was largely insensitive to DIDS inhibition. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a stimulation of loop-diuretic-insensitive 86Rb efflux across the basal-lateral surfaces. In addition, hypo-osmotic exposure of T84 cells is also associated with an increase in cytosolic Ca2+. It is concluded that the effects of hypo-osmotic exposure of T84 cells on secretory Isc are consistent with the activation of a DIDS-sensitive apical Cl- conductance and a basal-lateral K+ conductance. With prior activation of inward Isc by VIP via a cAMP-activated DIDS-insensitive apical Cl- conductance, augmentation of the secretory current by hypo-osmotic exposure is likely to result primarily from increased basal-lateral K+ current and loop-diuretic-sensitive Cl- uptake.",
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TY - JOUR

T1 - Characterisation of volume-activated ion transport across epithelial monolayers of human intestinal T84 cells

AU - McEwan, G T

AU - Brown, C D

AU - Hirst, B H

AU - Simmons, N L

PY - 1993/5

Y1 - 1993/5

N2 - The effects of hypo-osmolarity upon transepithelial ion transport in human intestinal cell layers have been investigated. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a transient stimulation of inward short-circuit current (Isc). This transient stimulation of inward current by hypo-osmotic media was abolished by 100 mumol/l 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS). After prestimulation of inward Isc by vasoactive intestinal peptide (VIP) or by combinations of carbachol and prostaglandin E1, hypo-osmotic exposure of the basal-lateral surfaces resulted in a further transient stimulation of Isc. The stimulation of Isc in these conditions was largely insensitive to DIDS inhibition. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a stimulation of loop-diuretic-insensitive 86Rb efflux across the basal-lateral surfaces. In addition, hypo-osmotic exposure of T84 cells is also associated with an increase in cytosolic Ca2+. It is concluded that the effects of hypo-osmotic exposure of T84 cells on secretory Isc are consistent with the activation of a DIDS-sensitive apical Cl- conductance and a basal-lateral K+ conductance. With prior activation of inward Isc by VIP via a cAMP-activated DIDS-insensitive apical Cl- conductance, augmentation of the secretory current by hypo-osmotic exposure is likely to result primarily from increased basal-lateral K+ current and loop-diuretic-sensitive Cl- uptake.

AB - The effects of hypo-osmolarity upon transepithelial ion transport in human intestinal cell layers have been investigated. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a transient stimulation of inward short-circuit current (Isc). This transient stimulation of inward current by hypo-osmotic media was abolished by 100 mumol/l 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS). After prestimulation of inward Isc by vasoactive intestinal peptide (VIP) or by combinations of carbachol and prostaglandin E1, hypo-osmotic exposure of the basal-lateral surfaces resulted in a further transient stimulation of Isc. The stimulation of Isc in these conditions was largely insensitive to DIDS inhibition. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a stimulation of loop-diuretic-insensitive 86Rb efflux across the basal-lateral surfaces. In addition, hypo-osmotic exposure of T84 cells is also associated with an increase in cytosolic Ca2+. It is concluded that the effects of hypo-osmotic exposure of T84 cells on secretory Isc are consistent with the activation of a DIDS-sensitive apical Cl- conductance and a basal-lateral K+ conductance. With prior activation of inward Isc by VIP via a cAMP-activated DIDS-insensitive apical Cl- conductance, augmentation of the secretory current by hypo-osmotic exposure is likely to result primarily from increased basal-lateral K+ current and loop-diuretic-sensitive Cl- uptake.

KW - 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid

KW - 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid

KW - Biological Transport

KW - Calcium

KW - Carbachol

KW - Cells, Cultured

KW - Chlorides

KW - Electric Conductivity

KW - Epithelium

KW - Humans

KW - Hypotonic Solutions

KW - Intestines

KW - Ions

KW - Kinetics

KW - Osmolar Concentration

KW - Prostaglandins E

KW - Rubidium Radioisotopes

KW - Vasoactive Intestinal Peptide

M3 - Article

VL - 423

SP - 213

EP - 220

JO - Pflugers Archiv : European Journal of Physiology

JF - Pflugers Archiv : European Journal of Physiology

SN - 0031-6768

IS - 3-4

ER -