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Acetylcholine (ACh) induces a K+ current in rabbit cardiac Purkinje fibres. The question was studied whether ACh produces this effect by modifying the properties of K+ channels pre-existing in the absence of the neurotransmitter or whether it induces the formation of a different type of K+ channels. The relaxation properties of the ACh-induced current and its blockade by Cs+ and Ba2+ have been investigated using voltage clamp. During hyperpolarizing or depolarizing voltage pulses of moderate amplitude, the ACh-induced current is time independent. For large voltage pulses, time-dependent changes of the ACh-induced current are observed. These latter changes can be explained by intracellular K+ accumulation/depletion phenomena or by the effects of ACh on time-dependent currents (e.g. the late outward current, ix). Cs+ and Ba2+ block the ACh-induced current. The block produced by 20 mM-Cs+ is instantaneous and increases with hyperpolarization, i.e. it is voltage dependent. The block produced by Ba2+ at high concentrations (greater than 1 mM) is also instantaneous but complete at all potentials studied, and thus voltage independent. At these concentrations, either ion also blocks the background inward rectifier (iK1) current in a similar way. Low [Ba2+] (less than 0.1 mM) cause a block of the ACh-induced current which is instantaneous and little voltage dependent. The block of iK1 in contrast is time and voltage dependent for the same concentrations. These results indicate that the ACh-induced K+ current is different from the background iK1 current.

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