高氯酸根离子对大鼠比目鱼肌纤维的作用。

Actions of perchlorate ions on rat soleus muscle fibres.

作者信息

Dulhunty A F, Zhu P H, Patterson M F, Ahern G

机构信息

Muscle Research Group, JCSMR, Australian National University, Canberra, ACT.

出版信息

J Physiol. 1992 Mar;448:99-119. doi: 10.1113/jphysiol.1992.sp019031.

DOI:10.1113/jphysiol.1992.sp019031

PMID:1317445

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1176189/

Abstract

The effects of perchlorate (ClO4-) on contraction have been studied in rat soleus muscle fibres using (i) potassium (K+) contracture and (ii) two-microelectrode-point voltage clamp techniques. 2. Membrane potentials (Vm) at all external [K+] were 3-5 mV more negative in ClO4-. The hyperpolarization could not be attributed to a change in Na+, K+, or Cl- permeability, or to an effect on the Na(+)-K+ pump. 3. ClO4- shifts the voltage dependence of tension activation, and contraction threshold, to more negative membrane potentials without altering maximum tension. Consequently, twitches and submaximal K+ contractures were potentiated, whereas tetanic contractions and 200 mM-K+ contractures were unaltered. 4. The decay of K+ contractures during steady depolarization with ClO4- developed a slow exponential phase with an average time constant of 6.05 +/- 0.76 min at -38 mV, and 1.68 +/- 0.15 min at -19 mV. This slow component was (a) under the rapid control of the surface Vm and (b) did not depend on external Ca2+. 5. Inactivation of E-C coupling was measured with a test 200 mM-K+ depolarization following 3-10 min depolarizations in conditioning solutions containing 20-120 mM-K+. ClO4- induced a negative shift in the curve-relating test K+ contracture amplitude to conditioning Vm but did not alter the rate of repriming of tension upon repolarization. 6. The results suggest that ClO4- increases the amount of activator produced during depolarization and thus allows the slow inactivation step in excitation-contraction (E-C) coupling to be reflected in the decay of K+ contracture tension. 7. A 'perchlorate contracture', which did not depend on the activation of E-C coupling, was observed. The contracture depended on external Ca2+, but not on voltage-dependent Ca2+ channels or Na(+)-Ca2+ exchange.

摘要

运用（i）钾（K⁺）挛缩和（ii）双微电极电压钳技术，研究了高氯酸盐（ClO₄⁻）对大鼠比目鱼肌纤维收缩的影响。2. 在所有外部[K⁺]浓度下，ClO₄⁻存在时膜电位（Vm）比正常情况负3 - 5 mV。这种超极化不能归因于Na⁺、K⁺或Cl⁻通透性的变化，也不能归因于对Na⁺ - K⁺泵的影响。3. ClO₄⁻将张力激活的电压依赖性和收缩阈值向更负的膜电位偏移，而不改变最大张力。因此，单收缩和次最大K⁺挛缩增强，而强直收缩和200 mM - K⁺挛缩未改变。4. 在ClO₄⁻存在下稳定去极化期间，K⁺挛缩的衰减出现一个缓慢的指数相，在 - 38 mV时平均时间常数为6.05±0.76分钟，在 - 19 mV时为1.68±0.15分钟。这个缓慢成分（a）受表面Vm的快速控制，（b）不依赖于外部Ca²⁺。5. 在含有20 - 120 mM - K⁺的条件溶液中进行3 - 10分钟去极化后，用200 mM - K⁺测试去极化测量兴奋 - 收缩（E - C）偶联的失活。ClO₄⁻导致测试K⁺挛缩幅度与条件Vm关系曲线出现负向偏移，但不改变复极化时张力再激发的速率。6. 结果表明，ClO₄⁻增加了去极化期间产生的激活剂数量，从而使兴奋 - 收缩（E - C）偶联中的缓慢失活步骤反映在K⁺挛缩张力的衰减中。7. 观察到一种不依赖于E - C偶联激活的“高氯酸盐挛缩”。这种挛缩依赖于外部Ca²⁺，但不依赖于电压依赖性Ca²⁺通道或Na⁺ - Ca²⁺交换。