Mechanically induced potentials in atrial fibroblasts from rat hearts are sensitive to hypoxia/reoxygenation.

Membrane potential changes of atrial fibroblasts in response to mechanical stress have been considered to modulate the rhythmic electrical activity of healthy hearts. Our recent findings suggest that cardiac arrhythmia after infarction is related to enhanced susceptibility of the fibroblasts to physical stretch. In this study, we analysed the effect of hypoxia/reoxygenation, which are major components of tissue ischemia/reperfusion, on the membrane potential of atrial fibroblasts. Intracellular microelectrode recordings were performed together with isometric force measurements on isometrically contracting right atrial tissue preparations from adult rats. Lowering the oxygen tension in the perfusate from 80 kPa to 3.5 kPa reduced active force development and decreased the resting membrane potential of the cardiac fibroblasts from -23+/-5 mV to -5+/-2 mV ( n=35). Application of gadolinium (40 microM) to inhibit non-selective cation channels prevented hypoxia-induced membrane depolarization of the fibroblasts. Reoxygenation of the myocardial tissue resulted in a transient increase of the resting membrane potential to maximally -60+/-8 mV. These findings indicate that transmembrane currents in atrial fibroblasts are sensitive to changes in tissue oxygenation. In conclusion, altered electro-mechanical function of the ischemic heart may possibly involve changes of the membrane potential of the cardiac fibroblasts.