Effect of H+ on ATP-regulated K+ channels in feline ventricular myocytes.

Effect of H+ on ATP-regulated K+ channels in feline ventricular myocytes.
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H 对猫心室肌细胞中 ATP 调节的 K 通道的影响。

DOI:
10.1152/ajpheart.1991.261.3.h755
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发表时间:
1991
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Kimura,S
Kimura,S
中科院分区:
--
文献类型:
--
作者:
Cuevas,J;Bassett,AL;Cameron,JS;Furukawa,T;Myerburg,RJ;Kimura,S

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采用膜片钳技术,研究了pH对猫左心室单个心肌细胞ATP调节的K+通道特性的影响。将由内而外贴片的ATP-K+通道双侧暴露于140 mM K+溶液(22 ℃)。在没有ATP和Mg 2+的情况下,在细胞内pH(pHi)7.4和6.5下,通道在超极化脉冲(20-100 mV,反向电位为负)期间具有线性电流-电压关系,但斜率电导在pHi 7.4时为66 +/-2 pS,在pHi 6.5时为46 +/- 2 pS。将pHi从7.4降至6.5增加了平均开放时间(从15.9 +/- 4.6降至35.9 +/- 7.9 ms,P <0.01),但降低了在50 mV正向反转电位下测量的开放状态概率(从0.35 +/- 0.04降至0.16 +/- 0.04,P <0.01)。然而,在0.2 mM ATP和1 mM MgCl 2存在下,将pHi从7.4降低到6.5增加了平均开放时间(从5.0 +/- 2.6到17.9 +/- 5.9 ms,P小于0.01)和开放状态概率(从0.025 +/- 0.010到0.098 +/- 0.024,P小于0.01)。这些数据表明,细胞内H+浓度的增加调节心脏ATP-K+通道特性。缺血相关的pHi降低可能会增强心脏ATP调节的K+通道的开放和由此产生的动作电位缩短。
Using patch-clamp techniques, we examined the effects of pH on properties of ATP-regulated K+ channels in single myocytes isolated from cat left ventricles. ATP-K+ channels of inside-out patches were bilaterally exposed to 140 mM K+ solutions (22 degrees C). In the absence of ATP and Mg2+, the channels had a linear current-voltage relationship during hyperpolarizing pulses (20-100 mV negative to the reversal potential) at both intracellular pH (pHi) 7.4 and 6.5, but the slope conductance was 66 +/- 2 pS at pHi 7.4 and 46 +/- 2 pS at pHi 6.5. Lowering pHi from 7.4 to 6.5 increased the mean open time (from 15.9 +/- 4.6 to 35.9 +/- 7.9 ms, P less than 0.01) but decreased the open-state probability measured at 50 mV positive to the reversal potential (from 0.35 +/- 0.04 to 0.16 +/- 0.04, P less than 0.01). However, in the presence of both 0.2 mM ATP and 1 mM MgCl2, lowering pHi from 7.4 to 6.5 increased the mean open time (from 5.0 +/- 2.6 to 17.9 +/- 5.9 ms, P less than 0.01) and the open-state probability (from 0.025 +/- 0.010 to 0.098 +/- 0.024, P less than 0.01). These data indicate that increases in intracellular H+ concentration modulate cardiac ATP-K+ channel properties. Ischemia-associated decreases in pHi may enhance the opening of cardiac ATP-regulated K+ channels and resultant action potential shortening.