Cardiac arrhythmias that occur in a wide variety of conditions where intracellular calcium is increased, have been attributed to the activation of a transient inward current (I_ti). I_ti is the result of three different [Ca]_i sensitive currents : the Na⁺/Ca²⁺ exchange, a Ca²⁺-activated chloride current and a Ca²⁺-activated non selective cationic current. Using the cell-free configuration of the patch-clamp technique, we have characterized the properties of a Ca²⁺-activated non-selective cation channel (NSC_Ca) in freshly dissociated human atrial cardiomyocytes. In excised inside-out patches, the channel presented a linear I/V relationship with a conductance of 19 ± 0.4 pS. It discriminated poorly among monovalent cations (Na⁺ and K⁺) and was slightly permeable to Ca²⁺ ions. The channel's open probability was increased by depolarisation and a rise in internal calcium, for which the K_d for [Ca²⁺]_i was 20.8 µM. Channel activity was reduced in the presence of 0.5 mM ATP or 10 µM glibenclamide on the cytoplasmic side to 22.1 ± 16.8 % and 28.5 ± 8.6 %, respectively, of control. It was also inhibited by 0.1 mM flufenamic acid. The channel shares several properties with TRPM4b and TRPM5, two members of the "TRP Melastatin" subfamily. In conclusion, the NSC_Ca channel is a serious candidate to support delayed after-depolarisations observed in [Ca²⁺] overload and thus should be implicated in the genesis of arrhythmias.