Kinetic studies of Ca2+ release from sarcoplasmic reticulum of normal and malignant hyperthermia susceptible pig muscles.
Kinetic studies of Ca2+ release from sarcoplasmic reticulum of normal and malignant hyperthermia susceptible pig muscles.
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正常和恶性高热易感猪肌肉肌浆网 Ca2 释放的动力学研究。
DOI：
10.1016/0005-2736(84)90187-1
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Ikemoto,N
中科院分区：
文献类型：
--
作者：
Kim,DH;Sreter,FA;Ohnishi,ST;Ryan,JF;Roberts,J;Allen,PD;Meszaros,LG;Antoniu,B;Ikemoto,N
使用停流分光光度法和胂III作为Ca 2+ 指示剂，研究了从正常猪和易患恶性高热的猪的肌肉中分离出的肌浆网中Ca 2+ 释放的时间过程。使用几种方法来触发Ca 2+ 释放：（a）添加氟烷（例如0.2 mM）；（b）增加囊外Ca 2+ 浓度（[Ca 0 2+]）；（c）（a）和（b）的组合，以及（d）离子（用氯化胆碱的葡萄糖酸钾）替代以产生膜去极化。由氟烷或单独的Ca 2+ 或两者诱导的Ca 2+ 释放的初始速率在恶性高热肌浆网中比正常情况下至少高70%。恶性高热肌浆网中氟烷在低[Ca 0 2+ ]时释放的Ca 2+ 量约为正常肌浆网的两倍。膜去极化导致恶性高热和正常肌浆网双相Ca 2+ 释放，膜去极化引起的Ca 2+ 快速释放速率常数在恶性高热肌浆网（k= 83 s− 1）中显着高于正常（k= 37 s− 1）。因此，所研究的所有类型的Ca 2+ 释放（a、b、c 和d）在恶性高热肌浆网中的比率高于正常肌浆网中的比率。这些结果表明，位于肌浆网中的推定Ca 2+ 释放通道在恶性高热肌浆网中发生了改变。
The time-course of Ca 2+ release from sarcoplasmic reticulum isolated from muscles of normal pigs and those of pigs susceptible to malignant hyperthermia were investigated using stopped-flow spectrophotometry and arsenazo III as a Ca 2+ indicator. Several methods were used to trigger Ca 2+ release:(a) addition of halothane (eg, 0.2 mM);(b) an increase of extravesicular Ca 2+ concentration ([Ca 0 2+]);(c) a combination of (a) and (b), and (d) replacement of ions (potassium gluconate with choline chloride) to produce membrane depolarization. The initial rates of Ca 2+ release induced by either halothane or Ca 2+ alone, or both, are at least 70% higher in malignant hyperthermic sarcoplasmic reticulum than in normal. The amount of Ca 2+ released by halothane at low [Ca 0 2+] in malignant hyperthermic sarcoplasmic reticulum is about twice as large as in normal sarcoplasmic reticulum. Membrane depolarization led to biphasic Ca 2+ release in both malignant hyperthermic and normal sarcoplasmic reticulum, the rate constant of the rapid phase of Ca 2+ release induced by membrane depolarization being significantly higher in malignant hyperthermic sarcoplasmic reticulum (k= 83 s− 1) than in normal (k= 37 s− 1). Thus, all types of Ca 2+ release investigated (a, b, c and d) have higher rates in malignant hyperthermic sarcoplasmic reticulum than normal sarcoplasmic reticulum. These results suggest that the putative Ca 2+ release channels located in the sarcoplasmic reticulum are altered in malignant hyperthermic sarcoplasmic reticulum.