Gordon A M, Godt R E
J Gen Physiol. 1970 Feb;55(2):254-75. doi: 10.1085/jgp.55.2.254.
In frog fast skeletal muscle, we find a decline of twitch, tetanus, and maximum K and caffeine contracture tensions as tonicity of the bathing solution is increased. The decline of tension independent of the method of producing contraction indicates that the major effect of hypertonicity is directly on contractile tension probably because of the increased internal ionic strength. However, there is some apparent disruption of excitation-contraction (E-C) coupling in solutions made three times the normal tonicity (3T solutions) since: (a) in 3T solutions tetanic and K contracture tensions decline to zero from a value near the average maximum caffeine contracture tension at this tonicity (10% of 1T tetanic tension). At this time, caffeine contractures of 10% of 1T tetanic tension can be elicited; (b) once the K contracture tension has declined, elevated Ca(++), 19.8 mM, restores K contracture tension to 13% of 1T tetanic tension. This probable disruption is not caused by changes in mechanical threshold since in 2T solutions the mechanical threshold is shifted by 12 mv in the hyperpolarizing direction. This is consistent with neutralization of fixed negative charges on the inside of the membrane. The repriming curve is also shifted in the hyperpolarizing direction in 2T solutions. Shifts of the repriming curve coupled with membrane depolarizations in 3T solutions (about 20 mv) may produce loss of repriming ability at the resting potential and disruption of E-C coupling.
在青蛙的快速骨骼肌中,我们发现随着浴液张力的增加,单收缩、强直收缩以及最大钾离子和咖啡因挛缩张力均下降。与产生收缩的方法无关的张力下降表明,高渗的主要作用可能是直接作用于收缩张力,这可能是由于内部离子强度增加所致。然而,在张力为正常三倍的溶液(3T溶液)中,兴奋-收缩(E-C)偶联存在一些明显的破坏,原因如下:(a)在3T溶液中,强直收缩和钾离子挛缩张力从接近该张力下平均最大咖啡因挛缩张力的值(1T强直张力的10%)降至零。此时,可以诱发1T强直张力10%的咖啡因挛缩;(b)一旦钾离子挛缩张力下降,将细胞外钙离子浓度升高至19.8 mM,可使钾离子挛缩张力恢复至1T强直张力的13%。这种可能的破坏并非由机械阈值的变化引起,因为在2T溶液中,机械阈值向超极化方向移动了12 mV。这与膜内侧固定负电荷的中和一致。在2T溶液中,再激发曲线也向超极化方向移动。3T溶液中再激发曲线的移动与膜去极化(约20 mV)相结合,可能导致静息电位下再激发能力丧失以及E-C偶联破坏。