RYANODINE MODIFIES CONDUCTANCE AND GATING BEHAVIOR OF SINGLE CA-2+ RELEASE CHANNEL
RYANODINE MODIFIES CONDUCTANCE AND GATING BEHAVIOR OF SINGLE CA-2+ RELEASE CHANNEL
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DOI：
10.1152/ajpcell.1987.253.3.c364
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发表时间：
1987-09-01
影响因子：
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通讯作者：
MEISSNER, G
中科院分区：
文献类型：
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作者：
ROUSSEAU, E;SMITH, JS;MEISSNER, G
兰尼定通过与肌浆网钙释放通道的特异性相互作用，影响骨骼肌和心肌的兴奋-收缩偶联。通过将骨骼和心脏SR囊泡掺入平面脂质双层，在单通道水平上研究了药物的作用。这两条通道分别被微摩尔游离钙离子和毫摩尔三磷酸腺苷激活，而被镁离子和钌红抑制。加入微摩尔浓度的兰诺定使钙离子和三磷酸腺苷激活的骨骼和心脏通道的单位电导降低约两倍。Ryanodine的第二个作用是增加通道的开放概率(Po)，使其在各种激活和失活条件下Po接近统一。兰诺定的作用是持久的，因为通过灌流去除兰诺定并不能使通道恢复其完全传导状态。
Ryanodine affects excitation-contraction coupling in skeletal and cardiac muscle by specifically interacting with the sarcoplasmic reticulum (SR) Ca2+ release channel. The effect of the drug at the single channel level was studied by incorporating skeletal and cardiac SR vesicles into planar lipid bilayers. The two channels were activated by micromolar free Ca2+ and millimolar ATP and inhibited by Mg2+ and ruthenium red. Addition of micromolar concentrations of ryanodine decreased about twofold the unit conductance of the Ca2+- and ATP-activated skeletal and cardiac channels. A second effect of ryanodine was to increase the open probability (Po) of the channels in such a way that Po was close to unity under a variety of activating and inactivating conditions. The effects of ryanodine were long lasting in that removal of ryanodine by perfusion did not return the channels into their fully conducting state.