, Volume 420, Issue 2, pp 180-186

Role of external Ca2+ and K+ in gating of cardiac delayed rectifier K+ currents

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We sought to determine whether extracellular Ca2+ (Ca e 2+ ) and K+ (K e + ) play essential roles in the normal functioning of cardiac K+ channels. Reports by others have shown that removal of Ca e 2+ and K e + alters the gating properties of neural delayed rectifier (I K) and A-type K+ currents, resulting in a loss of normal cation selectivity and voltage-dependent gating. We found that removal of Ca e 2+ and K e + from the solution bathing guinea pig ventricular myocytes often induced a leak conductance, but did not affect the ionic selectivity or time-dependent activation and deactivation properties of I K. The effect of [K+]e on the magnitude of the two components of cardiac I K was also examined. I K in guinea pig myocytes is comprised of two distinct types of currents: I Kr (rapidly activating, rectifying) and I Ks (slowly activating). The differential effect of Ca e 2+ on the two components of I K (previously shown to shift the voltage dependence of activation of the two currents in opposite directions) was exploited to determine the role of K e + on the magnitude of I Ks and I Kr. Lowering [K+]e from 4 to 0 mM increased I Ks, as expected from the change in driving force for K+, but decreased I Kr. The differential effect of [K+]e on the two components of cardiac I K may explain the reported discrepancies regarding modulation of cardiac I K conductance by this cation.