gms | German Medical Science

33rd International Congress on Electrocardiology

International Society of Electrocardiology

Effect of Angiotensin II and AT1-receptor blockade on Ca2+ homeostasis in human atrial myocytes as a model for the potential clinical benefit of AT-1 blockade in human atrial fibrillation

Meeting Abstract

  • corresponding author presenting/speaker M.C. Brandt - Klinik III für Innere Medizin, Köln, Germany
  • N. Gassanov - Klinik III für Innere Medizin, Köln, Germany
  • G. Michels - Klinik III für Innere Medizin, Köln, Germany
  • F. Er - Klinik III für Innere Medizin, Köln, Germany
  • U.C. Hoppe - Klinik III für Innere Medizin, Köln, Germany

33rd International Congress on Electrocardiology. Cologne, 28.06.-01.07.2006. Düsseldorf, Köln: German Medical Science; 2007. Doc06ice023

The electronic version of this article is the complete one and can be found online at:

Published: February 8, 2007

© 2007 Brandt et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



In chronic atrial fibrillation (AF) specific alterations of the myocardial structure, expression of ion channels and Ca2+ release from the sarcoplasmic reticulum have been demonstrated, underlying the clinical perpetuation of this condition. Moreover, local activation of the renin-angiotensin system (RAS) has recently been shown in atria during AF. To evaluate a potential role of angiotensin II (ANG II) in the pathophysiological changes of calcium handling in AF, we studied the effect of ANG II on the frequency and characteristics of Ca2+-sparks in human atrial myocytes. Single atrial myocytes were isolated from atrial appendages taken from patients in sinus rhythm and incubated in 1 µM ANG II or ANG II and the AT1-receptor blocker Candesartan. Ca2+ sparks were recorded with a confocal microscope in line-scan mode. In ANG II pretreated cells the frequency of spontaneously arising Ca2+ sparks was significantly higher than controls (44.9±3.8, n=33 vs. 14.0±2.0, n=38, 6 patients, p<0.001). This effect of ANG II was absent in the presence of Candesartan (13.9±2.3, n=32, p=NS vs. controls; p<0.001 vs. ANG II). The spark full duration was 127.3±10.2 ms in ANG II pretreated cells compared to 55.4±3.8 ms in controls (p<0.001), and 65.37±6.2 ms in ANG II plus Candesartan recordings (p<0.001 vs. ANG II). The time to peak Ca2+ fluorescence and decay time were significantly higher in the ANG II group compared to controls. These ANG II-mediated effects were completely prevented by Candesartan. The Ca2+ spark amplitude and SR Ca2+ content were similar in all groups. The observed ANG II induced alterations of calcium handling in human atrial cells were similar to those previously demonstrated in AF. Since these changes could be prevented by Candesartan, our data provide a molecular explanation for the clinical benefit of AT1-receptor blockade in the prevention and treatment of AF. Thus, blockade of the RAS might constitute a useful pharmacological strategy for patients with AF.