Mechanosensitivity is a widespread property of cells. In heart, it is associated with two main physiological and pathological situations: changes in blood filling and cell volume modifications. There is a lot of evidence that the sensors of changes in mechanical state are stretch-activated channels (SACs). In some cases, activation of SACs may lead to arrhythmias. However, it is of interest to note that the involvement of SACs in these arrhythmias are mainly based on indirect evidences such as their sensititvity to blockers like gadolinium (Gd³⁺) or streptomycin. But these blockers generally also block L-type calcium channels and it is also known that calcium plays an important role in the genesis of arrhythmias. Thus, it is not completely clear what is the involvement of these channels, even if admitted, in these pathologies. Pharmacological agents affecting specifically SACs would be of great interest for the study of strech-induced arrhythmias but also may provide a new class of antiarrhythmic drugs.