Na(+)‐K+ pump stimulation elicits recovery of contractility in K(+)‐paralysed rat muscle.
Na(+)‐K+ pump stimulation elicits recovery of contractility in K(+)‐paralysed rat muscle.
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Na(+)-K+ 泵刺激引起 K(+) 麻痹大鼠肌肉收缩力的恢复。
DOI：
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发表时间：
1993
期刊：
影响因子：
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通讯作者：
J. A. Flatman
中科院分区：
文献类型：
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作者：
T. Clausen;S. L. Andersen;J. A. Flatman
1.本研究探讨了主动的Na(+)-K+转运在高细胞外钾浓度([K+]o)下恢复大鼠比目鱼肌收缩力中的作用。这是使用已知的通过不同机制刺激Na(+)-K+泵的试剂(儿茶酚胺和胰岛素)完成的。2.在含有10 mM K+的Krebs-Ringer碳酸氢盐缓冲液中，完整肌肉的等长抽动和强直力下降40-69%。这种下降的主要部分可以通过添加沙丁胺醇(10(-5)M)来防止。在10 mM K+存在下，加入沙丁胺醇或肾上腺素和部分胰岛素可在5-10分钟内使肌力几乎完全恢复。3.在暴露于12.5 mM K+的肌肉中，力下降了96%。沙丁胺醇(10~(-5)M)、肾上腺素(10~(-6)M)和胰岛素(100 mU·L~(-1))在10~20min内恢复力值分别为57~71%、61~71%和38~47%。这些超过最大浓度的沙丁胺醇和胰岛素对力量恢复的影响是相加的。沙丁胺醇和肾上腺素在浓度降至10(-8)M时可显著恢复收缩能力(P<；0.005)。4.在比目鱼肌中，相同的药物刺激86Rb+摄取，降低细胞内Na+的摄取。这些作用反映了对主动Na(+)-K+转运的刺激，并且两者都与抽动和强直力的恢复呈高度显著的相关性(r=0.80-0.88；P<；0.001)。5.预先给予哇巴因(10~(-5)M×10分钟或10~(-3)M×1分钟)和河豚毒素(10~(-6)M)均可抑制沙丁胺醇、肾上腺素和胰岛素所致的肌力恢复。6.实验结果支持高[K+]o对骨骼肌收缩力的抑制作用可通过刺激主动的Na(+)-K+转运、细胞外K+清除量的增加和Na+的跨膜电化学梯度的增加而被抵消。
1. This study explores the role of active electrogenic Na(+)‐K+ transport in restoring contractility in isolated rat soleus muscles exposed to high extracellular potassium concentration ([K+]o). This was done using agents (catecholamines and insulin) known to stimulate the Na(+)‐K+ pump via different mechanisms. 2. When exposed to Krebs‐Ringer bicarbonate buffer containing 10 mM K+, the isometric twitch and tetanic force of intact muscles decreased by 40‐69%. The major part of this decline could be prevented by the addition of salbutamol (10(‐5) M). In the presence of 10 mM K+, force could be restored almost completely within 5‐10 min by the addition of salbutamol or adrenaline and partly by insulin. 3. In muscles exposed to 12.5 mM K+, force declined by 96%. Salbutamol (10(‐5) M), adrenaline (10(‐6) M) and insulin (100 mU ml‐1) produced 57‐71, 61‐71 and 38‐47% recovery of force within 10‐20 min, respectively. The effects of these supramaximal concentrations of salbutamol and insulin on force recovery were additive. Salbutamol and adrenaline produced significant recovery of contractility at concentrations down to 10(‐8) M (P < 0.005). 4. In soleus, the same agents stimulated 86Rb+ uptake and decreased intracellular Na+. These actions reflect stimulation of active Na(+)‐K+ transport and both showed a highly significant correlation to the recovery of twitch as well as tetanic force (r = 0.80‐0.88; P < 0.001). 5. The force recovery induced by salbutamol, adrenaline and insulin was suppressed by pre‐exposure to ouabain (10(‐5) M for 10 min or 10(‐3) M for 1 min) as well as by tetrodotoxin (10(‐6) M). 6. The observations support the conclusion that the inhibitory effect of high [K+]o on contractility in skeletal muscle can be counterbalanced by stimulation of active electrogenic Na(+)‐K+ transport, the ensuing increase in the clearance of extracellular K+ and in the transmembrane electrochemical gradient for Na+.