Hypotonic stress of cardiomyocytes leading to their swelling is considered as very important proarrhythmic event appearing during ischemia/reperfusion of heart. Experimental research work performed on isolated cardiomyocytes exposed to hypotonic solution identified the three typical changes in membrane potential during hypotonic challenge: 1) initial prolongation of APD, 2) secondary shortening of APD and 3) depolarization of membrane potential. There are several ionic currents activated by hypotonic stress: outwardly rectifying swelling-induced chloride currents (I_Cl,swell), inwardly rectifying non-selective cation currents (I_NSC) and slow component of delayed rectifier potassium currents (I_Ks) are some of them. However, membrane potential changes cannot be fully explained by reported ionic current changes. Limitation of methodological tools and complexity of the problem disable a complete resolving and clarification of this phenomenon. This mini-review will focus on membrane potential and current changes in cardiomyocytes induced only by cell swelling (not by cell inflation or mechanical stretch) and theirs clinical importance as potential proarrhythmic mechanisms.