The L-type Ca2+-channel subunits alpha1C and beta2 are not downregulated in atrial myocardium of patients with chronic atrial fibrillation.
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 Ca(2+) current (I(CaL)). 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 alpha1C and beta2 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 alpha1C and the beta2-subunit expression was not altered in atrial myocardium of AF patients. Also, the DHP-binding site density was unchanged.


CONCLUSIONS
The protein expression of the L-type Ca2+-channel subunits alpha1C or beta2 is not reduced in atrial myocardium of AF patients. Therefore, the reduced I(CaL) might be due to downregulation of other accessory subunits (alpha2delta), expression of aberrant subunits, changes in channel trafficking or alterations in channel function.
Department of Physiology, Maastricht University, PO Box 616 6200 MD, The, Maastricht, Netherlands. schotten@fys.unimaas.nl <schotten@fys.unimaas.nl>
Ulrich
U
Schotten
Hannelore
H
Haase
Dirk
D
Frechen
Maura
M
Greiser
Christoph
C
Stellbrink
Jaime F
JF
Vazquez-Jimenez
Ingo
I
Morano
Maurits A
MA
Allessie
Peter
P
Hanrath
D000818:Animals; D001281:Atrial Fibrillation / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D001665:Binding Sites; D020746:Calcium Channels, L-Type / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D002908:Chronic Disease; D004095:Dihydropyridines / Q000378:metabolism; D015536:Down-Regulation; D006801:Humans; D011485:Protein Binding; D011817:Rabbits
D020746:Calcium Channels, L-Type; D004095:Dihydropyridines; C038806:1,4-dihydropyridine