The effects of calcium deprivation upon mechanical and electrophysiological parameters in skeletal muscle fibres of the frog.
The effects of calcium deprivation upon mechanical and electrophysiological parameters in skeletal muscle fibres of the frog.
复制标题
缺钙对青蛙骨骼肌纤维机械和电生理参数的影响。
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
W. Spiecker
中科院分区：
文献类型：
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作者：
H. Lüttgau;W. Spiecker
1.研究了钙缺乏对青蛙半腱肌和髂腓肌单个肌纤维力学和电生理参数的影响。2.当外钙浓度从10~(-3)~10~(-9)M以一个数量级的步长递减时，加入10 mM-EGTA和3 mM-Mg~(2+)，K收缩的最大力下降5-15%，最大力平台缩短，大多数情况下自发松弛时相延长。3.在含有10(-9)M-Ca~(2+)和1 mM-Mg~(2+)的林格溶液中，85%的最大强直力可维持至少15秒(5赫兹；3℃)。4.外钙离子从10~(-3)M降至10~(-9)M，并被镁离子取代，使“稳态”失活曲线向更负的方向移动20-30 mV(这是指完全去极化时的最大力值与钾浓度或相应的膜电位的对数有关)。5.二价阳离子浓度的相同变化对激活曲线的形状和电位依赖性(最大力与相应膜电位的外部K浓度的对数有关)几乎没有影响。6.当外钙离子降至10(-9)M并被镁离子取代时，延迟整流开始的阈值电位(点电压钳)和启动动作电位的阈值电位没有变化。7.当EGTA2-浓度增加到80 mM(在5 mM-Mg2+存在的情况下)，抽动高度在几分钟内下降到很小的值。然而，在高EGTA2-中，1小时后仍可诱发出相当于原始值20-85%的50赫兹强直力。8.实验表明，外源性Ca~(2+)主要通过抑制“失活”作用于兴奋-收缩偶联。提出了一种假说，认为肌挛缩过程中最大力的平台是再生的依赖于Ca2+的失活曲线向更正的电位移动的结果。
1. The effects of Ca2+ deprivation upon mechanical and electrophysiological parameters of single muscle fibres from the m. semitendinosus and the m. iliofibularis of the frog were investigated. 2. When the external free Ca concentration was reduced in steps of one order of magnitude from 10(‐3) to 10(‐9) M, using up to 10 mM‐EGTA and in the presence of 3 mM‐Mg2+, the maximum force of K contractures declined by 5‐15%, the plateau of maximum force shortened, and in most cases the phase of spontaneous relaxation lengthened. 3. In Ringer solution containing 10(‐9) M‐Ca2+ and 1 mM‐Mg2+ 85% of maximum tetanic force could be maintained for at least 15 sec (5 Hz; 3 degrees C). 4. The reduction of external Ca2+ from 10(‐3) to 10(‐9) M and its replacement by Mg2+ induced a 20‐30 mV shift towards more negative potentials of the ‘steady state’ inactivation curve (which relates maximum force upon full depolarization to the logarithm of the K concentration or the corresponding membrane potential during the conditioning period). 5. The same alteration in concentrations of divalent cations caused little or no change in the shape and potential dependence of the activation curve (which relates maximum force to the logarithm of the external K concentration of the corresponding membrane potential). 6. The threshold potential for the onset of delayed rectification (point voltage clamp) and that for the initiation of an action potential did not change when external Ca2+ was reduced to 10(‐9) M and replaced by Mg2+. 7. When the concentration of EGTA2‐ was increased to 80 mM (in the presence of 5 mM‐Mg2+) twitch height dropped to very small values within a few minutes. However, tetanic force (50 Hz) reaching 20‐85% of the original value could still be induced after 1 hr in high EGTA2‐. 8. The experiments show that external Ca2+ acts upon excitation‐contraction coupling mainly by impeding ‘inactivation'. A hypothesis is proposed in which the plateau of maximum force during a contracture is the consequence of a regenerative Cai2+‐dependent shift of the inactivation curve towards more positive potentials.