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

在无钙条件下，对膜电位大于-20 mV的膜施加指令脉冲，可诱发瞬时外向电流(I_O)。这一电流在刺激后的几毫秒内达到峰值，然后以指数方式下降到时间常数为35ms的平台水平。该值不依赖于+10-+70 mV之间的膜电位，外加Cd^&lt；2+&gt；(0.1 mM)与Ca^&lt；2+&gt；向灌流液中加入D600(1µM)或奎尼丁(0.1 mM)对I_o产生可逆抑制，用四乙基铵(TEA)取代内K~+可完全抑制I_o，其稳态失活符合Boltzmann关系，其半钝化电压为-33.5 mV，斜率系数为7.5 mV。用4-氨基吡啶取代外部阳离子几乎完全抑制瞬时成分。刺激β-肾上腺素能对瞬变成分的波幅影响不大，但使平台成分的波幅增加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+)~(2+)正在掩盖A样钾通道的活动。这一发现提出了猪心脏A通道的功能表达在发育过程中可能发生改变的可能性。

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.