Author + information
- J. Neumann,
- U. Gergs,
- P. Kirchhof,
- L. Fabritz,
- F.U. Müller,
- K. Drzewiecki and
- P. Boknik
Although adenosine A2A-receptors (A2A-AR) are also present in the human heart, their role in arrhythmias is poorly understood.
We generated transgenic mice that overexpress A2A-AR in cardiac myocytes (TG) and compared them to littermate controls (WT).
In isolated cardiomyocytes from these hearts, the A2A-AR agonist CSG21680 led to a cAMP-increase and enhanced phosphorylation of regulatory proteins like phospholamban. In isolated right atrial preparations, we noted arrhythmias in 15 from 53 samples in WT but 27 from 57 samples of TG (χ2-test, p<0.05,). Moreover, in three from five isolated perfused hearts, we noted atrial arrhythmias but in none of eight perfused WT (χ2-test, p<0.05), consistent with enhanced atrial diameter in echocardiography of TG (n=9-12, p<0.05).
It is tempting to speculate that activation of A2A-AR might explain atrial fibrillation in some patients.