Cardiac fibroblasts can respond to mechanical deformation of the plasma membrane with characteristic changes of their membrane potential. These changes of fibroblasts membrane potential are determined by operation of stretch-inactivated channels. These channels, mainly permeable for sodium ions, are activated by compression of the cell leading to depolarization, and are inactivated by stretch, which in turn leads to hyperpolarization. Thus, cardiac fibroblasts function as mechanoelectric transducers in the heart and represent the cellular substrate for a cardiac mechanoelectrical feedback mechanism. Increased sensitivity of the cardiac fibroblasts to mechanical changes contributes to electrical instability and arrhythmia after myocardial infarction. Recent findings indicate that these processes involve the transfer of electrical signals via gap junctions. In this article we will discuss the recent progress in the electrophysiology of cardiac fibroblasts and their role in mechanoelectric feedback in healthy and diseased hearts.
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