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Ethanol Acutely Decreases Calcium Transients in Cultured Human Myotubes

Ethanol consumption frequently leads to a number of skeletal muscle disorders, including acute and chronic alcoholic myopathy. Ethanol has been found to interfere with signal transduction mechanisms in cardiac and smooth muscle cells. We studied the effects of ethanol on the intracellular calcium ([... Full description

Journal Title: Alcoholism: Clinical and Experimental Research August 1998, Vol.22(5), pp.1086-1092
Main Author: Nicolás, Josep M.
Other Authors: Antúnez, Emilia , Thomas, Andrew P. , Fernández‐Solá, Joaquim , Tobías, Ester , Estruch, Ramón , Urbano‐Márquez, Alvaro
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ID: ISSN: 0145-6008 ; E-ISSN: 1530-0277 ; DOI: 10.1111/j.1530-0277.1998.tb03705.x
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recordid: wj10.1111/j.1530-0277.1998.tb03705.x
title: Ethanol Acutely Decreases Calcium Transients in Cultured Human Myotubes
format: Article
creator:
  • Nicolás, Josep M.
  • Antúnez, Emilia
  • Thomas, Andrew P.
  • Fernández‐Solá, Joaquim
  • Tobías, Ester
  • Estruch, Ramón
  • Urbano‐Márquez, Alvaro
subjects:
  • Ethanol
  • Calcium
  • Excitation‐Contraction Coupling
  • Myotubes
ispartof: Alcoholism: Clinical and Experimental Research, August 1998, Vol.22(5), pp.1086-1092
description: Ethanol consumption frequently leads to a number of skeletal muscle disorders, including acute and chronic alcoholic myopathy. Ethanol has been found to interfere with signal transduction mechanisms in cardiac and smooth muscle cells. We studied the effects of ethanol on the intracellular calcium ([Ca]) transients responsible for excitation‐contraction coupling in human myotubes from chronic alcoholic patients and healthy controls. Cultured myotubes were loaded with the fluorescent Ca indicator fura‐2 and evaluated on a single‐cell basis. Following electrical stimulation, ethanol caused a significant reversible dose‐dependent reduction in [Ca], transient amplitude, achieving a mean decrease of 36 ± 5% at 300 mM ethanol (p < 0.01), without modifying the basal [Ca],. This acute effect of ethanol was similar in myotubes obtained from chronic alcoholics and controls. Similarly, ethanol caused a dose‐dependent reduction of [Ca], transient amplitude in control samples when depolarization was elicited by 100 mM KCl (p < 0.01). Several potential mechanisms of ethanol action were studied in control muscle samples. Sarcolemmal Ca entry was measured indirectly by monitoring Mn‐quenching of intracellular fura‐2 via the nitrendipine‐sensitive Ca channels during electrical pacing. Ethanol at doses of 100 mM and greater caused a dose‐dependent reduction in the rate of quench (p < 0.01). In addition, the intracellular pool of Ca releasable by caffeine was found to be reduced at 300 mM ethanol (p < 0.05). We conclude that ethanol reduces the [Ca], transients underlying excitation‐contraction coupling in human myotubes, and that this occurs to a similar extent in cells obtained from chronic alcoholics and controls. This acute effect of ethanol was primarily due to an inhibitory effect of ethanol on sarcolemmal Ca influx via voltage‐operated Ca channels, although there may also be an effect on the Ca sarcoplasmic reticulum loading state.
language:
source:
identifier: ISSN: 0145-6008 ; E-ISSN: 1530-0277 ; DOI: 10.1111/j.1530-0277.1998.tb03705.x
fulltext: fulltext
issn:
  • 0145-6008
  • 01456008
  • 1530-0277
  • 15300277
url: Link


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titleEthanol Acutely Decreases Calcium Transients in Cultured Human Myotubes
creatorNicolás, Josep M. ; Antúnez, Emilia ; Thomas, Andrew P. ; Fernández‐Solá, Joaquim ; Tobías, Ester ; Estruch, Ramón ; Urbano‐Márquez, Alvaro
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descriptionEthanol consumption frequently leads to a number of skeletal muscle disorders, including acute and chronic alcoholic myopathy. Ethanol has been found to interfere with signal transduction mechanisms in cardiac and smooth muscle cells. We studied the effects of ethanol on the intracellular calcium ([Ca]) transients responsible for excitation‐contraction coupling in human myotubes from chronic alcoholic patients and healthy controls. Cultured myotubes were loaded with the fluorescent Ca indicator fura‐2 and evaluated on a single‐cell basis. Following electrical stimulation, ethanol caused a significant reversible dose‐dependent reduction in [Ca], transient amplitude, achieving a mean decrease of 36 ± 5% at 300 mM ethanol (p < 0.01), without modifying the basal [Ca],. This acute effect of ethanol was similar in myotubes obtained from chronic alcoholics and controls. Similarly, ethanol caused a dose‐dependent reduction of [Ca], transient amplitude in control samples when depolarization was elicited by 100 mM KCl (p < 0.01). Several potential mechanisms of ethanol action were studied in control muscle samples. Sarcolemmal Ca entry was measured indirectly by monitoring Mn‐quenching of intracellular fura‐2 via the nitrendipine‐sensitive Ca channels during electrical pacing. Ethanol at doses of 100 mM and greater caused a dose‐dependent reduction in the rate of quench (p < 0.01). In addition, the intracellular pool of Ca releasable by caffeine was found to be reduced at 300 mM ethanol (p < 0.05). We conclude that ethanol reduces the [Ca], transients underlying excitation‐contraction coupling in human myotubes, and that this occurs to a similar extent in cells obtained from chronic alcoholics and controls. This acute effect of ethanol was primarily due to an inhibitory effect of ethanol on sarcolemmal Ca influx via voltage‐operated Ca channels, although there may also be an effect on the Ca sarcoplasmic reticulum loading state.
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titleEthanol Acutely Decreases Calcium Transients in Cultured Human Myotubes
descriptionEthanol consumption frequently leads to a number of skeletal muscle disorders, including acute and chronic alcoholic myopathy. Ethanol has been found to interfere with signal transduction mechanisms in cardiac and smooth muscle cells. We studied the effects of ethanol on the intracellular calcium ([Ca]) transients responsible for excitation‐contraction coupling in human myotubes from chronic alcoholic patients and healthy controls. Cultured myotubes were loaded with the fluorescent Ca indicator fura‐2 and evaluated on a single‐cell basis. Following electrical stimulation, ethanol caused a significant reversible dose‐dependent reduction in [Ca], transient amplitude, achieving a mean decrease of 36 ± 5% at 300 mM ethanol (p < 0.01), without modifying the basal [Ca],. This acute effect of ethanol was similar in myotubes obtained from chronic alcoholics and controls. Similarly, ethanol caused a dose‐dependent reduction of [Ca], transient amplitude in control samples when depolarization was elicited by 100 mM KCl (p < 0.01). Several potential mechanisms of ethanol action were studied in control muscle samples. Sarcolemmal Ca entry was measured indirectly by monitoring Mn‐quenching of intracellular fura‐2 via the nitrendipine‐sensitive Ca channels during electrical pacing. Ethanol at doses of 100 mM and greater caused a dose‐dependent reduction in the rate of quench (p < 0.01). In addition, the intracellular pool of Ca releasable by caffeine was found to be reduced at 300 mM ethanol (p < 0.05). We conclude that ethanol reduces the [Ca], transients underlying excitation‐contraction coupling in human myotubes, and that this occurs to a similar extent in cells obtained from chronic alcoholics and controls. This acute effect of ethanol was primarily due to an inhibitory effect of ethanol on sarcolemmal Ca influx via voltage‐operated Ca channels, although there may also be an effect on the Ca sarcoplasmic reticulum loading state.
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abstractEthanol consumption frequently leads to a number of skeletal muscle disorders, including acute and chronic alcoholic myopathy. Ethanol has been found to interfere with signal transduction mechanisms in cardiac and smooth muscle cells. We studied the effects of ethanol on the intracellular calcium ([Ca]) transients responsible for excitation‐contraction coupling in human myotubes from chronic alcoholic patients and healthy controls. Cultured myotubes were loaded with the fluorescent Ca indicator fura‐2 and evaluated on a single‐cell basis. Following electrical stimulation, ethanol caused a significant reversible dose‐dependent reduction in [Ca], transient amplitude, achieving a mean decrease of 36 ± 5% at 300 mM ethanol (p < 0.01), without modifying the basal [Ca],. This acute effect of ethanol was similar in myotubes obtained from chronic alcoholics and controls. Similarly, ethanol caused a dose‐dependent reduction of [Ca], transient amplitude in control samples when depolarization was elicited by 100 mM KCl (p < 0.01). Several potential mechanisms of ethanol action were studied in control muscle samples. Sarcolemmal Ca entry was measured indirectly by monitoring Mn‐quenching of intracellular fura‐2 via the nitrendipine‐sensitive Ca channels during electrical pacing. Ethanol at doses of 100 mM and greater caused a dose‐dependent reduction in the rate of quench (p < 0.01). In addition, the intracellular pool of Ca releasable by caffeine was found to be reduced at 300 mM ethanol (p < 0.05). We conclude that ethanol reduces the [Ca], transients underlying excitation‐contraction coupling in human myotubes, and that this occurs to a similar extent in cells obtained from chronic alcoholics and controls. This acute effect of ethanol was primarily due to an inhibitory effect of ethanol on sarcolemmal Ca influx via voltage‐operated Ca channels, although there may also be an effect on the Ca sarcoplasmic reticulum loading state.
copOxford, UK
pubBlackwell Publishing Ltd
doi10.1111/j.1530-0277.1998.tb03705.x
pages1086-1092
date1998-08