Fibroblasts in the heart can respond to mechanical deformation of the plasma membrane with characteristic changes of their membrane potential. Membrane depolarization of the fibroblasts occurs during the myocardial contractions and is caused by an influx of cations, mainly of sodium ions, into the cells. Conversely, application of mechanical stretch to the cells, i.e., during diastolic relaxation of the myocardium, will hyperpolarize the membrane potential of the fibroblasts due to reduced sodium entry. Thus, cardiac fibroblasts can function as mechano-electric transducers that are possibly involved in the mechano-electric feedback mechanism of the heart. Mechano-electric feedback refers to the phenomenon, that the cardiac mechanical environment, which depends on the variable filling pressure of the ventricles, modulates the electrical function of the heart. Increased sensitivity of the cardiac fibroblasts to mechanical forces may contribute to the electrical instability and arrhythmic disposition of the heart after myocardial infarction. Novel findings indicate that these processes involve the intercellular transfer of electrical signals between fibroblasts and cardiomyocytes via gap junctions. In this article we will discuss the recent progress in the electrophysiology of cardiac fibroblasts. The main focus will be on the intercellular pathways through which fibroblasts and cardiomyocytes communicate with each other.