Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

The L-type Ca2+ channel subunits alpha1c and beta2 are not downregulated in atrial myocardium of patients with chronic atrial fibrillation

Item Type:Article
Title:The L-type Ca2+ channel subunits alpha1c and beta2 are not downregulated in atrial myocardium of patients with chronic atrial fibrillation
Creators Name:Schotten, U. and Haase, H. and Frechen, D. and Greiser, M. and Stellbrink, C. and Vazguez-Jimenez, J.F. and Morano, I. and Allessie, M.A. and Hanrath, P.
Abstract:Objective. - Electrical remodeling as well as atrial contractile dysfunction after the conversion of atrial fibrillation (AF) to sinus rhythm (SR) are mainly caused by a reduction of the inward L-type Ca2+ current (ICaL). We investigated whether the expression of L-type Ca2+-channel subunits was reduced in atrial myocardium of AF patients. Methods. - Right atrial appendages were obtained from patients undergoing coronary artery bypass graft surgery (CAD, n = 35) or mitral valve surgery (MVD, n = 37). Seventeen of the CAD patients and 18 of the MVD patients were in chronic (>3 months) AF, whereas the others were in SR. The protein expression of the L-type Ca2+-channel subunits {alpha}1C and {beta}2 was quantified by western blot analysis. Furthermore, we measured the density of dihydropyridine (DHP)-binding sites of the L-type Ca2+ channel using 3H-PN220-100 as radioligand. Results. - Surprisingly, the {alpha}1C and the {beta}2-subunit expression was not altered in atrial myocardium of AF patients. Also, the DHP-binding site density was unchanged. Conclusion. - The protein expression of the L-type Ca2+-channel subunits {alpha}1C or {beta}2 is not reduced in atrial myocardium of AF patients. Therefore, the reduced ICaL might be due to downregulation of other accessory subunits ({alpha}2{delta}), expression of aberrant subunits, changes in channel trafficking or alterations in channel function.
Keywords:Arrhythmia, Atrial Fibrillation, Atrial Function, Ca Channel, Ion Channels, Remodeling
Source:Journal of Molecular and Cellular Cardiology
ISSN:0022-2828
Publisher:Elsevier (The Netherlands)
Volume:35
Number:5
Page Range:437-443
Date:May 2003
Official Publication:https://doi.org/10.1016/S0022-2828(03)00012-9
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library