Voltage-dependent inactivation of L-type Ca2+ currents in guinea-pig ventricular myocytes
Voltage-dependent inactivation of L-type Ca2+ currents in guinea-pig ventricular myocytes
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DOI：
10.1113/jphysiol.2002.029637
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发表时间：
2002-12-01
影响因子：
5.5
通讯作者：
Findlay, I
中科院分区：
文献类型：
--
作者：
Findlay, I
本研究的目的是描述天然心脏L型钙电流的电压依赖性失活的动力学。从豚鼠分离的心室肌细胞记录全细胞电流。通过用Mg 2+替代细胞外Ca 2+并记录通过Ca 2+通道的外向电流，将电压依赖性失活与Ca 2+依赖性失活分开。电压依赖性失活从-30 mV的缓慢双相衰减加速到+20 mV的最大快速双相衰减。最大的电压依赖性失活发生在tau（f）接近30 ms和tau（s）接近300 ms时，衰减的快成分占电流幅度的70%。在基础条件下，Ca ~（2+）电流有效性呈S形。异丙肾上腺素（异丙肾上腺素）诱发了大量增加的时间依赖性成分的Ca 2+电流，也增加了去极化。这是负责在正膜电位下的Ca 2+通道电流可用性的表观恢复，从而形成U形的可用性-电压（A-V）关系。结论是，β肾上腺素能刺激改变了天然心脏L型Ca 2+通道对膜电压的反应。在基础条件下，电压加速失活。在异丙肾上腺素，电压也可以减少失活。
The objective of this study was to describe the kinetics of voltage-dependent inactivation of native cardiac L-type Ca2+ currents. Whole-cell currents were recorded from guinea-pig isolated ventricular myocytes. Voltage-dependent inactivation was separated from Ca2+-dependent inactivation by replacing extracellular Ca2+ with Mg2+ and recording outward currents through Ca2+ channels. Voltage-dependent inactivation accelerated from slow monophasic decay at -30 mV to maximal rapid biphasic decay at +20 mV. Maximal voltage-dependent inactivation occurred with tau(f) similar to30 ms and tau(s) similar to300 ms, the fast component of decay accounted for 70% of the current amplitude. In basal conditions Ca2+ current availability was sigmoid. Isoproterenol (isoprenaline) evoked a large increase in a time-independent component of the Ca2+ current which also increased with depolarisation. This was responsible for the apparent recovery of Ca2+ channel current availability at positive membrane potentials and thus a U-shaped availability-voltage (A-V) relationship. It is concluded that, beta-adrenergic stimulation altered the reaction of native cardiac L-type Ca2+ channels to membrane voltage. In basal conditions, voltage accelerated inactivation. In isoproterenol, voltage could also reduce inactivation.