Physiological and pharmacological properties of A-like current evoked in Ca free solution and their developmental changes

在无Ca^2+条件下，对豚鼠心肌细胞施加一个大于-20 mV的膜电位指令脉冲，可引起瞬时外向电流（I_o）。该电流在刺激后的几毫秒内达到峰值，然后以35 ms的时间常数呈指数下降到一个平台水平。该值不依赖于+10 ~+70 mV的膜电位。在灌流液中加入D 600（1 μ M）或奎尼丁（0.1mM）可产生可逆的抑制作用，而用四乙基铵（TEA）替代内部K^+则可完全抑制I_o。瞬态成分的稳态失活可用Boltzmann关系表示，其半失活电压为-33.5mV，斜率因子为7.5mV。β-肾上腺素能刺激几乎没有改变瞬态分量的振幅，但增加了高原的2.7倍。我们认为，在豚鼠心肌细胞中，生理浓度的细胞外Ca^2+掩盖了A样K^+通道的活性。这一发现提出了一种可能性，即在豚鼠心脏中A通道的功能表达可能在发育过程中被修改。

Under Ca^<2+>-free conditions, transient outward currents (I_o)were elicited by application of a command pulse to membrane potentials more positive than -20 mV in the guinea-pig cardiac cell. This current reached a peak within a few milliseconds of stimulation, then decreased exponertially to a plateau level with a time constant of 35 ms. This value did not depend on the membrane potential between +10 and +70 mV.External Cd^<2+> (0.1mM) mimicked the inhibitory effect of Ca^<2+> on I_o. Addition of D600 (1muM) or quinidine (0.1mM) to the perfusate produced a reversible suppression, and replacement of internal K^+ with tetraethylammonium (TEA) induced a complete inhibition of I_o. The steady-state inactiveation of the transient component of I_o was expressed by a Boltzmann relation with a half-inactivation voltage of -33.5mV and a slope factor of 7.5mV.The transient component was almost was completely inhibited by substitution of 4- aminopyridine, but not TEA, for external cations. The beta adrenergic stimulation little altered an amplitude of the transient component, but increased that of the plateau 2.7 times. We suggest that in guinea-pig cardiac cells, extracellular Ca^<2+> at physiological concentrations is masking the activity of an A-like K^+ channel. This finding raises the possibility that the functional expression of A channels in the gunea-pig heart might be modified during the development.