Excitation-induced Ca2+ uptake in rat skeletal muscle
Excitation-induced Ca2+ uptake in rat skeletal muscle
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DOI：
10.1152/ajpregu.1999.276.2.r331
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发表时间：
1999-02-01
影响因子：
2.8
通讯作者：
Clausen, T
中科院分区：
文献类型：
--
作者：
Gissel, H;Clausen, T
在离体大鼠指长伸肌（EDL）进行等距收缩时，发现慢性低频电刺激导致Ca-45的摄取增加（240分钟后比对照高154%）和Ca2+的渐进式积累（240分钟后比对照高85%）。然而，在比目鱼中，这种处理导致了Ca-45摄取的少量但显著的增加（180分钟后比对照高30%），但没有显著的Ca2+积累。在没有任何外部负荷的等张收缩肌肉中，电刺激在EDL和比目鱼肌中引起更大的Ca-45摄取和Ca2+积累。这些Ca2+的吸收与Na+的积累相一致。在等长收缩或等张收缩期间，40 Hz的刺激使比目鱼肌Ca-45的初始（60秒）摄取速率分别增加了15倍和30倍。Ca2+通道阻滞剂硝苯地平和维拉帕米仅使刺激诱导的Ca-45摄取增加减少17%，但被河豚毒素阻断。刺激诱导的Na-22和Ca-45摄取的初始速率相关（r = 0.80; P < 0.003）。用缬草碱刺激Na+通道可使比目鱼和EDL对Ca-45的吸收分别增加93%和139% (P < 0.001)，而河豚毒素可消除这一作用。结果表明，在骨骼肌中，兴奋诱导大量Ca2+内流，由Na+通道介导。
In isolated rat extensor digitorum longus (EDL) muscle mounted for isometric contractions, chronic low-frequency electrical stimulation was found to lead to an increased uptake of Ca-45 (154% above control after 240 min) and a progressive accumulation of Ca2+ (85% above control after 240 min). In soleus, however, this treatment led to a small, but significant, increase in Ca-45 uptake (30% above control after 180 min) but no significant accumulation of Ca2+. In muscles mounted for isotonic contractions without any external load, electrical stimulation gave rise to a larger Ca-45 uptake and accumulation of Ca2+ in both EDL and soleus. These uptakes of Ca2+ coincided with an accumulation of Na+. During isometric or isotonic contractions, stimulation at 40 Hz increased the initial (60 s) rate of Ca-45 uptake in soleus muscle 15- and 30-fold, respectively. The stimulation-induced increase in Ca-45 uptake was only reduced by 17% by the Ca2+-channel blockers nifedipine and verapamil but was blocked by tetrodotoxin. The initial rate of stimulation-induced Na-22 and Ca-45 uptake was correlated (r = 0.80; P < 0.003). Stimulation of Na+ channels with veratridine increased Ca-45 uptake by 93 and 139% in soleus and EDL, respectively (P < 0.001), effects that were abolished by tetrodotoxin. The results indicate that in skeletal muscle, excitation induces a considerable influx of Ca2+, mediated by Na+ channels.