Calcium currents in isolated rabbit coronary arterial smooth muscle myocytes.
Calcium currents in isolated rabbit coronary arterial smooth muscle myocytes.
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离体兔冠状动脉平滑肌细胞中的钙电流。
DOI：
10.1113/jphysiol.1990.sp018192
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Shibata,EF
中科院分区：
文献类型：
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作者：
Matsuda,JJ;Volk,KA;Shibata,EF
1.使用单移液管电压钳技术记录来自兔心外膜左降支冠状动脉的松弛酶促分离平滑肌细胞的钙内向电流。用CsCl-四乙基铵填充的移液器溶液阻断Ouronik+电流。2.当浸泡在2.5 mM [Ca 2 +]o中时，松弛的冠状动脉平滑肌细胞具有8.6 +/-0.6微米的最大直径和96.7 +/-3.3微米的细胞长度。室温下的平均静息膜电位为-32 +/-10 mV。平均电池电容为18.5 +/-1.7 pF，输入电阻为3.79 +/-0.58 G Ω。3.从-80 mV的保持电位开始的去极化电压钳步骤引起单个时间和电压依赖性内向电流，该电流依赖于细胞外[Ca 2 +]。在2.5 mM [Ca 2 +]o中，内向电流在-40 mV的电位下被激活，并在+10 mV时达到峰值。该电流被0.5 mM-CdCl 2和1 μ M-硝苯地平抑制，并被1 μ M-Bay K 8644增强。未观察到可检测的低阈值、快速失活T型钙电流。4.在2.5 mM [Ca 2 +]o中，该内向电流的表观逆转电位为+70 mV，并且[Ca 2 +]o每增加10倍，该内向电流移动33.0 mV。该通道对钡离子和锶离子的渗透性也比对钙离子的渗透性高。5.使用110 mM-Ba 2+作为电荷载体的单钙通道记录显示平均斜率电导为20.7 +/-0.8 pS。6.这种钙电流（伊卡）表现出强烈的电压依赖性失活过程。然而，稳态灭活曲线（f无穷大）显示出对膜电位的轻微非单调U形依赖性。半数通道失活时的电位为-27.9 mV，斜率因子为6.9 mV。稳态激活曲线（d无穷大）也通过Boltzmann分布进行了良好描述，半激活电位为-4.4 mV，斜率因子为-63 mV。伊卡在约+20 mV时完全激活。7.失活速率取决于携带电流的离子种类。Sr ~（2+）和Ba ~（2+）均降低失活速率和失活程度。tau f（拟合的失活时间常数）曲线在2.5 mM [Ca 2 +]o中显示U形关系。再激活过程是电压依赖性的，可以用一个单一的指数来描述。8.电流幅值和失活动力学具有温度依赖性。（400字处截断摘要）
1. Calcium inward currents were recorded from relaxed enzymatically isolated smooth muscle cells from the rabbit epicardial left descending coronary artery using a single‐pipette voltage‐clamp technique. Outward K+ currents were blocked with CsCl‐tetraethylammonium‐filled pipette solutions. 2. Relaxed coronary smooth muscle cells had a maximum diameter of 8.6 +/‐ 0.6 microns and a cell length of 96.7 +/‐ 3.3 microns when bathed in 2.5 mM [Ca2+]o. The average resting membrane potential at room temperature was ‐32 +/‐ 10 mV. The mean cell capacitance was 18.5 +/‐ 1.7 pF and the input resistance was 3.79 +/‐ 0.58 G omega. 3. Depolarizing voltage‐clamp steps from a holding potential of ‐80 mV elicited a single time‐ and voltage‐dependent inward current which was dependent upon extracellular [Ca2+]. In 2.5 mM [Ca2+]o, the inward current was activated at a potential of ‐40 mV and peaked at +10 mV. This current was inhibited by 0.5 mM‐CdCl2 and 1 microM‐nifedipine and was enhanced with 1 microM‐Bay K 8644. No detectable low‐threshold, rapidly inactivating T‐type calcium current was observed. 4. The apparent reversal potential of this inward current in 2.5 mM [Ca2+]o was +70 mV and shifted by 33.0 mV per tenfold increase in [Ca2+]o. This channel was also more permeable to barium and strontium ions than to calcium ions. 5. Single calcium channel recordings with 110 mM‐Ba2+ as the charge carrier revealed a mean slope conductance of 20.7 +/‐ 0.8 pS. 6. This calcium current (ICa) exhibited a strong voltage‐dependent inactivation process. However, the steady‐state inactivation curve (f infinity) displayed a slight nonmonotonic, U‐shaped dependence upon membrane potential. The potential at which half of the channels were inactivated was ‐27.9 mV with a slope factor of 6.9 mV. The steady‐state activation curve (d infinity) was also well‐described by a Boltzmann distribution with a half‐activation potential at ‐4.4 mV and a slope factor of ‐63 mV. ICa was fully activated at approximately +20 mV. 7. The rate of inactivation was dependent upon the species of ion carrying the current. Both Sr2+ and Ba2+ decreased the rate as well as the degree of inactivation. The tau f (fitted time constant of inactivation) curve displayed a U‐shaped relationship in 2.5 mM [Ca2+]o. The reactivation process was voltage dependent and could be described by a single exponential. 8. The current amplitude and the inactivation kinetics were temperature dependent.(ABSTRACT TRUNCATED AT 400 WORDS)