Inward rectifier K+ currents in smooth muscle cells from rat coronary arteries: Block by Mg2+, Ca2+, and Ba2+
Inward rectifier K+ currents in smooth muscle cells from rat coronary arteries: Block by Mg2+, Ca2+, and Ba2+
复制标题
DOI：
10.1152/ajpheart.1996.271.2.h696
复制
发表时间：
1996-08-01
影响因子：
4.8
通讯作者：
Nelson, MT
中科院分区：
文献类型：
--
作者：
Robertson, BE;Bonev, AD;Nelson, MT
内向整流钾通道参与了膜电位的调控和外部钾离子诱导的小冠状动脉扩张。为了识别和表征冠状动脉平滑肌的内向整流钾电流，在常规和穿孔配置的膜片钳技术中测量从大鼠冠状动脉（间隔）动脉（直径，100-150 μ m）酶分离的平滑肌细胞的全细胞钾电流。Ba 2+敏感，全细胞K+电流-电压关系表现出内向整流。平滑肌中的Ca 2+激活K+通道（1 mM四乙基铵离子）、ATP敏感性K+通道（10 μ M格列本脲）和电压依赖性K+通道（1 mM 4-氨基吡啶）的阻滞剂不影响内向整流K+电流。非选择性K+通道抑制剂苯环利定（100 μ M）减少内向整流K+电流的50%。外部Ba 2+减少内向电流，与膜电位超极化增加抑制。在-60 mV时，Ba 2+的半抑制常数为2.1 μ M，在25 mV超极化时降低e倍。外部Cs+也阻断内向整流K+电流，在-60 mV时Cs+的半抑制常数为2.9 mM。外源性Ca ~（2+）和Mg ~（2+）均降低内向整流钾电流。在-60 mV时，Ca 2+和Mg 2+（1 mM）分别使内向电流降低33%和21%。向内整流不受透析的细胞的内部与名义上的Ca 2+和Mg 2 +-免费的解决方案。提示冠状动脉平滑肌存在内向整流性钾通道，Ba ~（2+）可作为研究内向整流性钾通道功能的探针。
Inward rectifier K+ channels have been implicated in the control of membrane potential and external K+-induced dilations of small coronary arteries. To identify and characterize inward rectifier K+ currents in coronary artery smooth muscle, whole cell K+ currents in smooth muscle cells enzymatically isolated from rat coronary (septal) arteries (diameters, 100-150 mu m) were measured in the conventional and perforated configurations of the patch-clamp technique. Ba2+-sensitive, whole cell K+ current-voltage relationships exhibited inward rectification. Blockers of Ca2+-activated K+ channels (1 mM tetraethylammonium ion), ATP-sensitive K+ channels (10 mu M glibenclamide), and voltage-dependent K+ channels (1 mM 4-aminopyridine) in smooth muscle did not affect inward rectifier K+ currents. The nonselective K+ channel inhibitor phencyclidine (100 mu M) reduced inward rectifier K+ currents by similar to 50%. External Ba2+ reduced inward currents, with membrane potential hyperpolarization increasing inhibition. The half-inhibition constant for Ba2+ was 2.1 mu M at -60 mV, decreasing e-fold for a 25-mV hyperpolarization. External Cs+ also blocked inward rectifier K+ currents, with the half-inhibition constant for Cs+ of 2.9 mM at -60 mV. External Ca2+ and Mg2+ reduced inward rectifier K+ currents. At -60 mV, Ca2+ and Mg2+ (1 mM) reduced inward currents by 33 and 21%, respectively. Inward rectification was not affected by dialysis of the cell's interior with a nominally Ca2+- and Mg2+-free solution. These findings indicate that inward rectifier K+ channels exist in coronary artery smooth muscle and that Ba2+ may be a useful probe for the functional role of inward rectifier K+ channels in coronary arteries.