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

Background: Excessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. L‐type Ca 2+ channels, involved in excitation–contraction coupling, are disturbed in animal models of persistent ethanol consumption. This study was designed to evaluate...

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Published inAlcoholism, clinical and experimental research Vol. 31; no. 7; pp. 1099 - 1105
Main Authors Fatjó, Francesc, Sancho‐Bru, Pau, Fernández‐Solà, Joaquim, Sacanella, Emilio, Estruch, Ramón, Bataller, Ramón, Nicolás, Josep‐María
Format Journal Article
LanguageEnglish
Published 01.07.2007
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ISSN0145-6008
1530-0277
DOI10.1111/j.1530-0277.2007.00404.x

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Summary:Background: Excessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. L‐type Ca 2+ 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 2+ channel receptors in organ donors with chronic alcoholism and controls. Methods: The protein expression of L‐type Ca 2+ channels was determined with 3 H‐(+)‐PN 200‐110‐binding experiments using a specific antibody against the α 1 ‐subunit in homogenate samples of left‐ventricle apex from organ donors: healthy controls ( n =11), chronic alcoholic without cardiomyopathy ( n =12), and alcoholics with cardiomyopathy ( n =11). Morphometric measurements of cardiomyocytes were performed. Results: Binding experiments proved an up‐regulation of L‐type Ca 2+ channels expression in alcoholic patients compared with controls ( B max 2.61 ± 1.10 vs 1.33 ± 0.49 fmol/mg, respectively; p <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; p =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 μ m 2 , respectively; p <0.001 both) as was the perimeter (78.7 ± 7.7 vs 61.5 ± 7.2 and 56.5 ± 2.8 μ m, respectively; p <0.001 both). Binding results did not change after adjusting receptor measurements for cross‐sectional area and cell perimeter. Conclusions: Chronic alcoholism causes an up‐regulation of myocardial L‐type Ca 2+ channel receptors, which decreases when cardiomyopathy is present.
ISSN:0145-6008
1530-0277
DOI:10.1111/j.1530-0277.2007.00404.x