The delayed rectifier potassium current (IK) initiates action potential repolarization in embryonic chick atrial cells, but an additional IX1 component is required for complete repolarization.
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Findings in embryonic chick cells leave open IX1 contributions to repolarization in mammalian models; further validation required.
We have measured the delayed rectifier potassium current, IK, with the whole-cell patch-clamp technique from single cultured cells from the atria of 6- to 11-day-old chick embryonic hearts. 2. The IK component was activated with depolarizing voltage-clamp steps positive to -30 mV (holding potential in the -60 to -40 mV range). Maximum activation of the IK conductance occurred at +25 mV, based on deactivation, or tail current amplitudes upon return to the holding potential. Activation and tail current kinetics could both be described by single-exponential functions of time. 3. The IK kinetics were voltage dependent, with a maximum time constant, tau n, of approximately 2 s at V = -20 mV. 4. The IK reversal potential measurements suggest that this current is carried predominantly by potassium ions. 5. The IK results from single cells, or clusters of two or three cells, were comparable to our recent measurements of IK (IX2) in heart cell aggregates (Shrier & Clay, 1986). However, we did not obtain clear evidence in single cells for the IX1 repolarization current, in contrast to the aggregate results. 6. Computer simulations based on our IK measurements demonstrate that this component is sufficient to initiate repolarization of the action potential in single cells. However, it is not sufficient to reproduce the latter phase of repolarization for potentials negative to -30 mV. Addition of a relatively small IX1 component (2% in absolute terms compared to the aggregate work) is sufficient to account for this part of the action potential.
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Clay et al. (1988) studied this question.
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