Uehara A, Yasukochi M, Imanaga I
Department of Physiology, School of Medicine, Fukuoka University, Japan.
J Mol Cell Cardiol. 1994 Feb;26(2):195-202. doi: 10.1006/jmcc.1994.1022.
The modulating effects of Ca2+ on single K+ channel currents in canine heart sarcoplasmic reticulum were studied using a planar lipid bilayer technique. The open-state probability and the unitary open-state current both decreased gradually as the Ca2+ concentration was reduced from pCa 3 to pCa 7.5. Each single-channel I-V curve was ohmic at any pCa: the modulating effect of Ca2+ within this range was voltage independent. The Ca2+ dose-response curves for the conductances and open probabilities were all biphasic in shape for both sides of the channel at the voltages used. However, Ca2+ within the pCa ranges used caused significantly more prominent activation of conductance and gating properties on the cytoplasmic side than it did on the SR luminal side. Furthermore, conductance decreased when cytoplasmic Ca2+ concentrations were greater than pCa 3. The I-V relation in this instance exhibited inward rectification caused by a voltage-dependent fast block. This suggests that cardiac SR K+ channel currents may be activated or inhibited through various types of Ca2+ binding sites on and within the channels.
采用平面脂双层技术研究了Ca2+对犬心脏肌浆网中单个K+通道电流的调节作用。当Ca2+浓度从pCa 3降低到pCa 7.5时，开放态概率和单通道开放态电流均逐渐降低。在任何pCa下，每条单通道I-V曲线均呈欧姆特性：在此范围内Ca2+的调节作用与电压无关。在所使用的电压下，通道两侧电导和开放概率的Ca2+剂量反应曲线均呈双相。然而，在所使用的pCa范围内，Ca2+对胞质侧电导和门控特性的激活作用明显比肌浆网腔侧更显著。此外，当胞质Ca2+浓度大于pCa 3时，电导降低。在这种情况下，I-V关系表现为电压依赖性快速阻滞引起的内向整流。这表明心脏肌浆网K+通道电流可能通过通道上和通道内的各种类型Ca2+结合位点被激活或抑制。
