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