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À propos de : Characterization of a [Ca2+]i-dependent current in human atrial and ventricular cardiomyocytes in the absence of Na+ and K+        

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  • Characterization of a [Ca2+]i-dependent current in human atrial and ventricular cardiomyocytes in the absence of Na+ and K+
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  • Abstract. Objectives: In situations of [Ca2+]i-overload, arrhythmias are believed to be triggered by delayed afterdepolarizations, which are generated by a transient inward current ITI. This study was designed to examine [Ca2+]i-dependent membrane currents in the absence of the Na+/Ca2+-exchanger as possible contributors to ITI in human cardiac cells. Methods: The whole cell voltage clamp technique was used for electrophysiological measurements in human atrial and ventricular cardiomyocytes. [Ca2+]i-measurements were performed using the fluorescent Ca2+-indicator fura-2. All solutions were Na+-free. Voltage-independent [Ca2+]i-transients were elicited by rapid caffeine applications. Results: In atrial myocytes, caffeine induced a transient membrane current in the absence of Na+ and K+. This current could be suppressed by internal EGTA (10 mM). Cl− did not contribute to this current. Experiments with different cations suggested non-selectivity for Cs+ and Li+, whereas N-methyl-d-glucamine appeared to be impermeable. Voltage ramps indicated a linear current-voltage relation in the range of +80 to −80 mV. Fluorescence measurements revealed a dissociation between the time courses of current and bulk [Ca2+]i-signal. In ventricular cardiomyocytes, caffeine failed to induce transient currents in 54 cells from 22 different patients with or without terminal heart failure. Conclusions: In human atrial cardiomyocytes, a [Ca2+]i-dependent nonspecific cation channel is expressed and may contribute to triggered arrhythmias in situations of [Ca2+]i-overload. No evidence could be found for the existence of a [Ca2+]i-dependent chloride current in atrial cells. In ventricular cells, neither a [Ca2+]i-dependent nonspecific cation channel nor a [Ca2+]i-dependent chloride channel seems to be expressed. Possible delayed afterdepolarizations in human ventricular myocardium might therefore be carried by the Na+/Ca2+-exchanger alone.
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  • 41-1-175
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