Role of external Ca2+ and K+ in gating of cardiac delayed rectifier K+ currents
- Cite this article as:
- Sanguinetti, M.C. & Jurkiewicz, N.K. Pflügers Arch. (1992) 420: 180. doi:10.1007/BF00374988
We sought to determine whether extracellular Ca2+ (Cae2+) and K+ (Ke+) play essential roles in the normal functioning of cardiac K+ channels. Reports by others have shown that removal of Cae2+and Ke+alters the gating properties of neural delayed rectifier (IK) and A-type K+ currents, resulting in a loss of normal cation selectivity and voltage-dependent gating. We found that removal of Cae2+and Ke+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 IK. The effect of [K+]e on the magnitude of the two components of cardiac IK was also examined. IK in guinea pig myocytes is comprised of two distinct types of currents: IKr (rapidly activating, rectifying) and IKs (slowly activating). The differential effect of Cae2+on the two components of IK (previously shown to shift the voltage dependence of activation of the two currents in opposite directions) was exploited to determine the role of Ke+on the magnitude of IKs and IKr. Lowering [K+]e from 4 to 0 mM increased IKs, as expected from the change in driving force for K+, but decreased IKr. The differential effect of [K+]e on the two components of cardiac IK may explain the reported discrepancies regarding modulation of cardiac IK conductance by this cation.