Effect of intracellular Ca2+ and action potential duration on L-type Ca2+ channel inactivation and recovery from inactivation in rabbit cardiac myocytes
Effect of intracellular Ca2+ and action potential duration on L-type Ca2+ channel inactivation and recovery from inactivation in rabbit cardiac myocytes
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DOI：
10.1152/ajpheart.00469.2006
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发表时间：
2007-07-01
影响因子：
4.8
通讯作者：
Bers, Donald M.
中科院分区：
文献类型：
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作者：
Altamirano, Julio;Bers, Donald M.
Ca2+ 电流 (I-Ca) 从失活状态恢复对于正常的心脏兴奋-收缩耦合是必要的。在正常心脏中，增加刺激频率会增加力，但在心力衰竭 (HF) 中，这种力-频率关系 (FFR) 通常会变平或逆转。虽然肌浆网 Ca2+-ATP 酶功能降低可能与此有关，但 ICa 可用性降低也可能有所贡献。心力衰竭时较长的动作电位持续时间 (APD)、较慢的细胞内 Ca2+ 浓度 ([Ca2+](i)) 下降以及较高的舒张压 [Ca2+](i) 都可能减慢 ICa 从失活状态的恢复，从而降低 ICa 的可用性。我们测量了不同舒张压 [Ca2+](i) 对兔心肌细胞 ICa 失活和失活恢复的影响。测量了 ICa 和 Ba2+ 电流 (I-Ba)。 ICa 衰减仅在高舒张压 [Ca2+](i) (600 nM) 下加速。 IBa 失活较慢，但对 [Ca2+](i) 不敏感。 ICa 或 IBa 可用性的膜电位依赖性不受 [Ca2+](i) 的影响
Ca2+ current (I-Ca) recovery from inactivation is necessary for normal cardiac excitation-contraction coupling. In normal hearts, increased stimulation frequency increases force, but in heart failure (HF) this force-frequency relationship (FFR) is often flattened or reversed. Although reduced sarcoplasmic reticulum Ca2+-ATPase function may be involved, decreased ICa availability may also contribute. Longer action potential duration (APD), slower intracellular Ca2+ concentration ([Ca2+](i)) decline, and higher diastolic [Ca2+](i) in HF could all slow ICa recovery from inactivation, thereby decreasing ICa availability. We measured the effect of different diastolic [Ca2+](i) on ICa inactivation and recovery from inactivation in rabbit cardiac myocytes. Both ICa and Ba2+ current (I-Ba) were measured. ICa decay was accelerated only at high diastolic [Ca2+](i) (600 nM). IBa inactivation was slower but insensitive to [Ca2+](i). Membrane potential dependence of ICa or IBa availability was not affected by [Ca2+](i)