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Up‐Regulation of Myocardial L‐Type Ca 2+ Channel in Chronic Alcoholic Subjects Without Cardiomyopathy

Excessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. L‐type Ca channels, involved in excitation–contraction coupling, are disturbed in animal models of persistent ethanol consumption. This study was designed to evaluate the density an... Full description

Journal Title: Alcoholism: Clinical and Experimental Research July 2007, Vol.31(7), pp.1099-1105
Main Author: Fatjó, Francesc
Other Authors: Sancho‐Bru, Pau , Fernández‐Solà, Joaquim , Sacanella, Emilio , Estruch, Ramón , Bataller, Ramón , Nicolás, Josep‐María
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ID: ISSN: 0145-6008 ; E-ISSN: 1530-0277 ; DOI: 10.1111/j.1530-0277.2007.00404.x
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recordid: wj10.1111/j.1530-0277.2007.00404.x
title: Up‐Regulation of Myocardial L‐Type Ca 2+ Channel in Chronic Alcoholic Subjects Without Cardiomyopathy
format: Article
creator:
  • Fatjó, Francesc
  • Sancho‐Bru, Pau
  • Fernández‐Solà, Joaquim
  • Sacanella, Emilio
  • Estruch, Ramón
  • Bataller, Ramón
  • Nicolás, Josep‐María
subjects:
  • Ethanol
  • Myocardium
  • Calcium Channels
  • Alcoholic Cardiomyopathy
ispartof: Alcoholism: Clinical and Experimental Research, July 2007, Vol.31(7), pp.1099-1105
description: Excessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. L‐type Ca channels, involved in excitation–contraction coupling, are disturbed in animal models of persistent ethanol consumption. This study was designed to evaluate the density and function of myocardial L‐type Ca channel receptors in organ donors with chronic alcoholism and controls. The protein expression of L‐type Ca channels was determined with H‐(+)‐PN 200‐110‐binding experiments using a specific antibody against the ‐subunit in homogenate samples of left‐ventricle apex from organ donors: healthy controls (=11), chronic alcoholic without cardiomyopathy (=12), and alcoholics with cardiomyopathy (=11). Morphometric measurements of cardiomyocytes were performed. Binding experiments proved an up‐regulation of L‐type Ca channels expression in alcoholic patients compared with controls ( 2.61 ± 1.10 vs 1.33 ± 0.49 fmol/mg, respectively;
language:
source:
identifier: ISSN: 0145-6008 ; E-ISSN: 1530-0277 ; DOI: 10.1111/j.1530-0277.2007.00404.x
fulltext: fulltext
issn:
  • 0145-6008
  • 01456008
  • 1530-0277
  • 15300277
url: Link


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titleUp‐Regulation of Myocardial L‐Type Ca 2+ Channel in Chronic Alcoholic Subjects Without Cardiomyopathy
creatorFatjó, Francesc ; Sancho‐Bru, Pau ; Fernández‐Solà, Joaquim ; Sacanella, Emilio ; Estruch, Ramón ; Bataller, Ramón ; Nicolás, Josep‐María
ispartofAlcoholism: Clinical and Experimental Research, July 2007, Vol.31(7), pp.1099-1105
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subjectEthanol ; Myocardium ; Calcium Channels ; Alcoholic Cardiomyopathy
descriptionExcessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. L‐type Ca channels, involved in excitation–contraction coupling, are disturbed in animal models of persistent ethanol consumption. This study was designed to evaluate the density and function of myocardial L‐type Ca channel receptors in organ donors with chronic alcoholism and controls. The protein expression of L‐type Ca channels was determined with H‐(+)‐PN 200‐110‐binding experiments using a specific antibody against the ‐subunit in homogenate samples of left‐ventricle apex from organ donors: healthy controls (=11), chronic alcoholic without cardiomyopathy (=12), and alcoholics with cardiomyopathy (=11). Morphometric measurements of cardiomyocytes were performed. Binding experiments proved an up‐regulation of L‐type Ca channels expression in alcoholic patients compared with controls ( 2.61 ± 1.10 vs 1.33 ± 0.49 fmol/mg, respectively; <0.001). This up‐regulation was present in the group of alcoholic subjects without cardiomyopathy, and was not seen in those with cardiomyopathy (3.39 ± 2.20 vs 1.77 ± 0.53 fmol/mg, respectively; =0.02). The cross‐sectional area and perimeter of the cells were greater in alcoholic patients with cardiomyopathy compared with controls and alcoholic patients without cardiomyopathy (500 ± 87 vs 307 ± 74 and 255 ± 25 m, respectively; <0.001 both) as was the perimeter (78.7 ± 7.7 vs 61.5 ± 7.2 and 56.5 ± 2.8 m, respectively; <0.001 both). Binding results did not change after adjusting receptor measurements for cross‐sectional area and cell perimeter. Chronic alcoholism causes an up‐regulation of myocardial L‐type Ca channel receptors, which decreases when cardiomyopathy is present.
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titleUp‐Regulation of Myocardial L‐Type Ca 2+ Channel in Chronic Alcoholic Subjects Without Cardiomyopathy
descriptionExcessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. L‐type Ca channels, involved in excitation–contraction coupling, are disturbed in animal models of persistent ethanol consumption. This study was designed to evaluate the density and function of myocardial L‐type Ca channel receptors in organ donors with chronic alcoholism and controls. The protein expression of L‐type Ca channels was determined with H‐(+)‐PN 200‐110‐binding experiments using a specific antibody against the ‐subunit in homogenate samples of left‐ventricle apex from organ donors: healthy controls (=11), chronic alcoholic without cardiomyopathy (=12), and alcoholics with cardiomyopathy (=11). Morphometric measurements of cardiomyocytes were performed. Binding experiments proved an up‐regulation of L‐type Ca channels expression in alcoholic patients compared with controls ( 2.61 ± 1.10 vs 1.33 ± 0.49 fmol/mg, respectively; <0.001). This up‐regulation was present in the group of alcoholic subjects without cardiomyopathy, and was not seen in those with cardiomyopathy (3.39 ± 2.20 vs 1.77 ± 0.53 fmol/mg, respectively; =0.02). The cross‐sectional area and perimeter of the cells were greater in alcoholic patients with cardiomyopathy compared with controls and alcoholic patients without cardiomyopathy (500 ± 87 vs 307 ± 74 and 255 ± 25 m, respectively; <0.001 both) as was the perimeter (78.7 ± 7.7 vs 61.5 ± 7.2 and 56.5 ± 2.8 m, respectively; <0.001 both). Binding results did not change after adjusting receptor measurements for cross‐sectional area and cell perimeter. Chronic alcoholism causes an up‐regulation of myocardial L‐type Ca channel receptors, which decreases when cardiomyopathy is present.
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abstractExcessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. L‐type Ca channels, involved in excitation–contraction coupling, are disturbed in animal models of persistent ethanol consumption. This study was designed to evaluate the density and function of myocardial L‐type Ca channel receptors in organ donors with chronic alcoholism and controls. The protein expression of L‐type Ca channels was determined with H‐(+)‐PN 200‐110‐binding experiments using a specific antibody against the ‐subunit in homogenate samples of left‐ventricle apex from organ donors: healthy controls (=11), chronic alcoholic without cardiomyopathy (=12), and alcoholics with cardiomyopathy (=11). Morphometric measurements of cardiomyocytes were performed. Binding experiments proved an up‐regulation of L‐type Ca channels expression in alcoholic patients compared with controls ( 2.61 ± 1.10 vs 1.33 ± 0.49 fmol/mg, respectively; <0.001). This up‐regulation was present in the group of alcoholic subjects without cardiomyopathy, and was not seen in those with cardiomyopathy (3.39 ± 2.20 vs 1.77 ± 0.53 fmol/mg, respectively; =0.02). The cross‐sectional area and perimeter of the cells were greater in alcoholic patients with cardiomyopathy compared with controls and alcoholic patients without cardiomyopathy (500 ± 87 vs 307 ± 74 and 255 ± 25 m, respectively; <0.001 both) as was the perimeter (78.7 ± 7.7 vs 61.5 ± 7.2 and 56.5 ± 2.8 m, respectively; <0.001 both). Binding results did not change after adjusting receptor measurements for cross‐sectional area and cell perimeter. Chronic alcoholism causes an up‐regulation of myocardial L‐type Ca channel receptors, which decreases when cardiomyopathy is present.
copMalden, USA
pubBlackwell Publishing Inc
doi10.1111/j.1530-0277.2007.00404.x
pages1099-1105
date2007-07