Bretylium causes a K+-Na+ pump activation that is independent of Na+ H+ exchange in depolarized rat, mouse and human lymphocytes

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Abstract

We have studied a bretylium tosylate induced increase of the membrane potentials of partially depolarized rat, mouse and human lymphocytes, using the potential sensitive dye, bis [1,3, dibutylbarbituric acid-(5) trimethine oxonol]. The extent of this repolarization is dose-dependent and decreased in magnitude as the temp was reduced from 37°C to room temp. The repolarizing effect is inhibited by K+-Na+-pump blockers or lack of extracellular Na+. Sodium ion channel blockers are effective in abolishing repolarization only if applied prior to, or simultaneously with, bretylium. Activation of Na+ H+ exchange is not involved in the mechanism of the phenomenon as the latter is completely eliminated in the presence of 10μM amiloride (concn of the diuretics having no measurable inhibition on the action of the exchanger). These data suggest that bretylium opens ligand- and voltage-gated Na+ channels, and repolarization occurs due to higher activity of the K+-Na+-pump stimulated by the enhanced intracellular Na+ accumulation.

Original languageEnglish
Pages (from-to)1307-1311
Number of pages5
JournalMolecular Immunology
Volume27
Issue number12
DOIs
Publication statusPublished - 1990

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Bretylium Tosylate
Sodium Channel Blockers
Lymphocytes
Sodium Channels
Amiloride
Diuretics
Membrane Potentials
Coloring Agents
Ligands
Acids
bretylium

ASJC Scopus subject areas

  • Molecular Biology
  • Immunology

Cite this

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title = "Bretylium causes a K+-Na+ pump activation that is independent of Na+ H+ exchange in depolarized rat, mouse and human lymphocytes",
abstract = "We have studied a bretylium tosylate induced increase of the membrane potentials of partially depolarized rat, mouse and human lymphocytes, using the potential sensitive dye, bis [1,3, dibutylbarbituric acid-(5) trimethine oxonol]. The extent of this repolarization is dose-dependent and decreased in magnitude as the temp was reduced from 37°C to room temp. The repolarizing effect is inhibited by K+-Na+-pump blockers or lack of extracellular Na+. Sodium ion channel blockers are effective in abolishing repolarization only if applied prior to, or simultaneously with, bretylium. Activation of Na+ H+ exchange is not involved in the mechanism of the phenomenon as the latter is completely eliminated in the presence of 10μM amiloride (concn of the diuretics having no measurable inhibition on the action of the exchanger). These data suggest that bretylium opens ligand- and voltage-gated Na+ channels, and repolarization occurs due to higher activity of the K+-Na+-pump stimulated by the enhanced intracellular Na+ accumulation.",
author = "L. Tr{\'o}n and Carlo Pieri and T. M{\'a}ri{\'a}n and L. Balkay and M. Emri and S. Damjanovich",
year = "1990",
doi = "10.1016/0161-5890(90)90035-X",
language = "English",
volume = "27",
pages = "1307--1311",
journal = "Molecular Immunology",
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TY - JOUR

T1 - Bretylium causes a K+-Na+ pump activation that is independent of Na+ H+ exchange in depolarized rat, mouse and human lymphocytes

AU - Trón, L.

AU - Pieri, Carlo

AU - Márián, T.

AU - Balkay, L.

AU - Emri, M.

AU - Damjanovich, S.

PY - 1990

Y1 - 1990

N2 - We have studied a bretylium tosylate induced increase of the membrane potentials of partially depolarized rat, mouse and human lymphocytes, using the potential sensitive dye, bis [1,3, dibutylbarbituric acid-(5) trimethine oxonol]. The extent of this repolarization is dose-dependent and decreased in magnitude as the temp was reduced from 37°C to room temp. The repolarizing effect is inhibited by K+-Na+-pump blockers or lack of extracellular Na+. Sodium ion channel blockers are effective in abolishing repolarization only if applied prior to, or simultaneously with, bretylium. Activation of Na+ H+ exchange is not involved in the mechanism of the phenomenon as the latter is completely eliminated in the presence of 10μM amiloride (concn of the diuretics having no measurable inhibition on the action of the exchanger). These data suggest that bretylium opens ligand- and voltage-gated Na+ channels, and repolarization occurs due to higher activity of the K+-Na+-pump stimulated by the enhanced intracellular Na+ accumulation.

AB - We have studied a bretylium tosylate induced increase of the membrane potentials of partially depolarized rat, mouse and human lymphocytes, using the potential sensitive dye, bis [1,3, dibutylbarbituric acid-(5) trimethine oxonol]. The extent of this repolarization is dose-dependent and decreased in magnitude as the temp was reduced from 37°C to room temp. The repolarizing effect is inhibited by K+-Na+-pump blockers or lack of extracellular Na+. Sodium ion channel blockers are effective in abolishing repolarization only if applied prior to, or simultaneously with, bretylium. Activation of Na+ H+ exchange is not involved in the mechanism of the phenomenon as the latter is completely eliminated in the presence of 10μM amiloride (concn of the diuretics having no measurable inhibition on the action of the exchanger). These data suggest that bretylium opens ligand- and voltage-gated Na+ channels, and repolarization occurs due to higher activity of the K+-Na+-pump stimulated by the enhanced intracellular Na+ accumulation.

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U2 - 10.1016/0161-5890(90)90035-X

DO - 10.1016/0161-5890(90)90035-X

M3 - Article

VL - 27

SP - 1307

EP - 1311

JO - Molecular Immunology

JF - Molecular Immunology

SN - 0161-5890

IS - 12

ER -