Activation of contraction in cat ventricular myocytes: effects of low Cd(2+) concentration and temperature.
Activation of contraction in cat ventricular myocytes: effects of low Cd(2+) concentration and temperature.
复制标题
猫心室肌细胞收缩的激活：低 Cd(2) 浓度和温度的影响。
DOI：
10.1152/ajpheart.1999.277.2.h488
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Vites,AM
中科院分区：
文献类型：
--
作者：
Wasserstrom,JA;Vites,AM
使用 Cd2+ (20 μM) 和不同浴温的影响来研究两种独立的触发机制（L 型 Ca2+ 电流 (ICa) 和反向模式 Na+/Ca2+ 交换）对猫心室肌细胞兴奋-收缩 (E-C) 耦合的贡献。使用充满含 K+ 内部溶液的贴片移液器和不连续（“开关”）电压钳研究离子电流和细胞缩短。灌注Cd2+可阻断细胞缩短，这与ICa的阻断密切相关； Cd2+诱导的收缩减少的电压依赖性呈钟形，在测试电位低于-10 mV和高于+50 mV时显示最小值，在约+20 mV时显示最大值。 Cd2+ 不敏感细胞缩短可被兰尼碱 (10 μM) 和 Ni2+(4–5 mM) 阻断。当动作电位用作电压钳（动作电位钳）的命令波形时，Cd2+将收缩减少至对照细胞缩短的～60±7%（n=7）。剩余的收缩被兰尼丁和 Ni2+ 阻断。硝苯地平 (10 μM) 的灌注引起与 Cd2+ 几乎相同的效果。收缩的电压依赖性在高于 34°C 时呈 S 形，但在低于 30°C 时呈钟形。当将 Cd2+ 添加到超融合液中时，收缩在 25°C 时被消除（至对照的 6 ± 3%），但在 34°C 时仅适度减少（至对照的 65 ± 13%，测试电位 +10 mV，n= 4，P< 0.01）。这些结果表明：1）存在对ICa拮抗剂敏感的收缩成分，并且该阻滞与有机或无机拮抗剂等效；2）在我们的实验条件下，Na+/Ca2+交换对触发收缩的贡献在整个测试电压范围内是相当线性的；3）ICa的贡献叠加在Na+/Ca2+交换剂贡献的背景成分上； 4) 通过交换器的触发与温度相关，在生理温度下提供主要贡献，但在低于 30°C 的温度下以几乎全有或全无的方式失效。
The effects of Cd2+(20 μM) and different bath temperatures were used to study the contributions of two separate triggering mechanisms, L-type Ca2+current (ICa) and reverse mode Na+/Ca2+exchange, to excitation-contraction (E-C) coupling in cat ventricular myocytes. Ionic currents and cell shortening were studied with patch pipettes filled with K+-containing internal solution and discontinuous (“switch”) voltage clamp. Superfusion with Cd2+blocked cell shortening that closely mirrored the block ofICa; the voltage dependence of Cd2+-induced reduction in contraction was bell-shaped, displaying minima at test potentials below −10 mV and above +50 mV and a maximum at about +20 mV. Cd2+-insensitive cell shortening was blocked by ryanodine (10 μM) and Ni2+(4–5 mM). When an action potential was used as the command waveform for the voltage clamp (action potential clamp), Cd2+reduced contraction to ∼60 ± 7% of control cell shortening (n= 7). The remaining contraction was blocked by ryanodine and Ni2+. Superfusion with nifedipine (10 μM) caused nearly identical effects to Cd2+. The voltage dependence of contraction was sigmoidal at temperatures above 34°C but bell-shaped below 30°C. When Cd2+was added to superfusate, contraction was abolished at 25°C (to 6 ± 3% of control) but reduced only modestly at 34°C (to 65 ± 13% of control, test potential +10 mV,n= 4,P< 0.01). These results indicate that1) there is a component of contraction that is sensitive toICaantagonists, and the block is equivalent with either organic or inorganic antagonists;2) the contribution of Na+/Ca2+exchange to triggering of contraction under our experimental conditions is fairly linear throughout the entire voltage range tested;3) the contribution ofICais superimposed on this background component contributed by the Na+/Ca2+exchanger; and4) triggering via the exchanger is temperature-dependent, providing a major contribution at physiological temperatures but failing at temperatures below 30°C in a nearly all-or-none fashion.