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Am J Physiol Heart Circ Physiol 282: H842-H849, 2002. First published October 11, 2001; doi:10.1152/ajpheart.00240.2001
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Vol. 282, Issue 3, H842-H849, March 2002

A possible role for atrial fibroblasts in postinfarction bradycardia

Andre Kamkin1,3, Irina Kiseleva1,3, Kay-Dietrich Wagner1, Alexander Pylaev1, Kate P. Leiterer2, Heinz Theres2, Holger Scholz1, Joachim Günther1, and Gerrit Isenberg3

1 Institute of Physiology and 2 Clinic of Internal Medicine I, Humboldt-University, Charité, 10117 Berlin; and 3 Department of Physiology, Martin-Luther-University of Halle, 0697 Halle/Saale, Germany

Atrial fibroblasts are considered to modulate the contractile activity of the heart in response to mechanical stretch. In this study we examined whether atrial fibroblasts are possibly involved in bradyarrhythmia, which is a severe complication after myocardial infarction. For this purpose, transmembrane electrical potentials were recorded in cardiac fibroblasts near the sinoatrial node from sham-operated rats and from rats with myocardial infarction. Twenty days after infarction due to coronary artery ligation, the right atrial tissue weights and the sensitivity of the fibroblast membrane potential to mechanical stretch correlated positively with the infarct size. Cardiac growth was enhanced, but the stretch sensitivity and the resting membrane potential of the atrial fibroblasts declined between 8 and 30 days after infarction. The frequency of spontaneous atrial contractions was significantly reduced 8 days after myocardial infarction and recovered in parallel with the membrane potential of the fibroblasts. These findings suggest that changes in the susceptibility of atrial fibroblasts to mechanical stretch may contribute to bradyarrhythmia during postinfarct remodeling of the heart.

cardiac hypertrophy; stretch-activated ion channels; mechanotransduction; membrane potential; gadolinium


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