TY - JOUR
T1 - Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue
AU - Olsen, Kristine B
AU - Braunstein, Thomas H
AU - Sørensen, Charlotte M
AU - Axelsen, Lene Nygaard
AU - Holstein-Rathlou, Niels-Henrik
AU - Nielsen, Morten S
PY - 2011/10
Y1 - 2011/10
N2 - Aim. Atrial angiotensin II (Ang II) levels are increased in atrial fibrillation and are believed to be important in the pathogenesis of atrial arrhythmias. Ang II reduces intercellular coupling by inhibiting gap junctions (connexins) and may thereby increase the risk of reentry arrhythmia. The aim of the current study was to investigate the acute effect of Ang II on conduction velocity (CV) in atrial tissue from normal and chronically infarcted rats. Methods. Contractile force was measured and CV was determined from the conduction time between electrodes placed on the tissue preparation. Expression of AT1a and AT1b receptors was examined by real-time PCR. Results. Acute stimulation with Ang II did not affect CV in tissue from auricle or atrial free wall. A transient 6.5 ± 3.6% increase in resting tension was observed in atrial free wall preparations, indicating that receptors are present and functional in the free wall preparation. The difference between free wall and auricle was probably not caused by differences in receptor expression since equal amounts of AT1 mRNA were present. To test if myocardial infarction (MI) sensitizes the atrium to Ang II, free atrial wall from rats subjected to 45 weeks ventricular MI was examined. Although CV was significantly reduced by MI, no effect on CV of Ang II was seen. Conclusion. Ang II does not acutely regulate CV in tissue preparations from the free wall of the left atria or the left auricle. Although ventricular MI reduces CV, this does not sensitize the atria to Ang II.
AB - Aim. Atrial angiotensin II (Ang II) levels are increased in atrial fibrillation and are believed to be important in the pathogenesis of atrial arrhythmias. Ang II reduces intercellular coupling by inhibiting gap junctions (connexins) and may thereby increase the risk of reentry arrhythmia. The aim of the current study was to investigate the acute effect of Ang II on conduction velocity (CV) in atrial tissue from normal and chronically infarcted rats. Methods. Contractile force was measured and CV was determined from the conduction time between electrodes placed on the tissue preparation. Expression of AT1a and AT1b receptors was examined by real-time PCR. Results. Acute stimulation with Ang II did not affect CV in tissue from auricle or atrial free wall. A transient 6.5 ± 3.6% increase in resting tension was observed in atrial free wall preparations, indicating that receptors are present and functional in the free wall preparation. The difference between free wall and auricle was probably not caused by differences in receptor expression since equal amounts of AT1 mRNA were present. To test if myocardial infarction (MI) sensitizes the atrium to Ang II, free atrial wall from rats subjected to 45 weeks ventricular MI was examined. Although CV was significantly reduced by MI, no effect on CV of Ang II was seen. Conclusion. Ang II does not acutely regulate CV in tissue preparations from the free wall of the left atria or the left auricle. Although ventricular MI reduces CV, this does not sensitize the atria to Ang II.
KW - Faculty of Health and Medical Sciences
U2 - 10.3109/00365513.2011.589009
DO - 10.3109/00365513.2011.589009
M3 - Journal article
C2 - 21728898
SN - 0085-591X
VL - 71
SP - 492
JO - Scandinavian Journal of Clinical and Laboratory Investigation. Supplement
JF - Scandinavian Journal of Clinical and Laboratory Investigation. Supplement
IS - 6
ER -