In bullfrog atrial muscle, instantaneous outward current is modified by Na-Ca exchange mechanisms, and delayed outward current consists of components susceptible to Na and Ca ions.
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No immediate clinical implications; leaves open whether Na-Ca exchange modulates Ik1 or delayed rectifier currents in mammalian or human atrium.
Effects of Ca-free or Na-deficient Ringer solutions on the membrane currents of the bullfrog atrial muscle were studied using the double sucrose-gap method. Instantaneous outward current (Ik1) decreased in Ca-free and increased in Na-deficient conditions. The amplitude of nominal "fully activated delayed outward current" diminished under both sets of conditions. The diminution, however, was greater in Na-deficient medium (10 mM Na) and its activation curve shifted about 13.5 mV toward a more negative potential. In Ca-free Ringer, no such shift was observed, and the activation of the delayed outward current became slower and sigmoidal while the deactivation was faster than in the control. Contrarily, in Na-deficient Ringer, the activation became faster and exponential and the deactivation was slower. The current tail was composed of two exponentially declining components, and the slower, K-accumulation-related component (Ia) was suppressed in Ca-free and the faster component (Ixs) diminished in Na-deficient media. These findings may indicate that in the atrial muscle the instantaneous outward current is modified by a Na-Ca exchange mechanisms and that the delayed outward current consists of two components, Ixs and Ia, which are susceptible to Na and Ca ions, respectively.
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GOTO et al. (1982) studied this question.
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