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兔骨骼肌中电荷移动的组成部分:丁卡因和硝苯地平的作用。

Components of charge movement in rabbit skeletal muscle: the effect of tetracaine and nifedipine.

作者信息

Lamb G D

出版信息

J Physiol. 1986 Jul;376:85-100. doi: 10.1113/jphysiol.1986.sp016143.

Abstract

The effects of tetracaine and nifedipine on asymmetric charge movement in rabbit muscle fibres were examined to investigate whether mammalian charge movement could be subdivided into several components. Tetracaine (0.05-0.2 mM) stopped contraction in every sternomastoid fibre examined (n = 9) and reduced the asymmetric charge (moved by depolarizing steps to 0 mV) by 15% (S.E. of mean 3%). Tetracaine had little effect on the charge moved at potentials more negative than the threshold potential (established in the absence of the drug). Application of the Ca2+ channel blocker nifedipine (2 or 10 microM), reduced the mean maximum asymmetric charge to 50% (+/- 4) of the control value in twenty-three sternomastoid fibres and to 32% (+/- 5) in four soleus fibres. Increasing the concentration of nifedipine to 120 microM had little further effect. The charge moved at potentials more negative than -60 mV was unaffected by nifedipine. A similar result was found with 30 microM-D600 (two fibres). 10 microM-nifedipine completely blocked Ca2+ currents (external [Ca2+] = 8 mM), but 0.15 microM-nifedipine only had a small effect on either the Ca2+ current or charge movement in the four fibres examined. Contractions could no longer be elicited in eleven of eighteen fibres within 6 min of the application of 2 or 10 microM-nifedipine. However, in the remaining seven fibres contractions could be elicited with unchanged thresholds over 30 min, even in the presence of 50 microM-nifedipine. Nifedipine did not noticeably effect q gamma. It is suggested that nifedipine might prevent contraction only when, for other reasons, the normal release of Ca2+ from the sarcoplasmic reticulum has been disrupted and contraction is dependent on the inflow of external Ca2+. The amount of asymmetric charge moved by depolarizing steps was about 50% greater with a holding potential of -110 mV than with one of -90 mV. This 'extra' charge was not suppressed by nifedipine.

摘要

研究了丁卡因和硝苯地平对兔肌纤维不对称电荷移动的影响,以探讨哺乳动物的电荷移动是否可细分为几个成分。丁卡因(0.05 - 0.2 mM)使所检查的每一条胸锁乳突肌纤维(n = 9)停止收缩,并使不对称电荷(通过去极化至0 mV步骤移动)减少15%(平均标准误3%)。丁卡因对在比阈电位(在无药物时确定)更负的电位下移动的电荷影响很小。应用钙通道阻滞剂硝苯地平(2或10 μM),使23条胸锁乳突肌纤维的平均最大不对称电荷降至对照值的50%(±4),4条比目鱼肌纤维降至32%(±5)。将硝苯地平浓度增加到120 μM进一步影响不大。在比 - 60 mV更负的电位下移动的电荷不受硝苯地平影响。用30 μM - D600(两条纤维)也得到了类似结果。10 μM硝苯地平完全阻断钙电流(细胞外[Ca2 +] = 8 mM),但0.15 μM硝苯地平对所检查的4条纤维中的钙电流或电荷移动仅有微小影响。在应用2或10 μM硝苯地平后6分钟内,18条纤维中有11条不再能引发收缩。然而,在其余7条纤维中,即使存在50 μM硝苯地平,在30分钟内仍能以不变的阈值引发收缩。硝苯地平对qγ没有明显影响。提示硝苯地平可能仅在由于其他原因肌浆网中Ca2 +的正常释放受到破坏且收缩依赖于细胞外Ca2 +流入时才会阻止收缩。去极化步骤移动的不对称电荷量在 - 110 mV的钳制电位下比在 - 90 mV时大约大50%。这种“额外”电荷不受硝苯地平抑制。

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