Ma T S, Bose D
Am J Physiol. 1977 Jan;232(1):C59-66. doi: 10.1152/ajpcell.1977.232.1.C59.
The contraction of guinea-pig taenia coli due to high K+ could not be reversed by washing when Na+ was absent from the medium. Reintroduction of Na+ (7 mM or more) caused relaxation. Similar results were obtained with rat uterus. The effect of sodium replacement was not due to change in ionic strength because equal or higher osmoles of choline, Ca++, K+, Mn++, or Mg++ had little or no effect. Persistence of contraction in the Na+-free medium was not due to a "catch state" of the contractile apparatus. Impairment of Ca+ removal from the cytoplasm rather than persistent increase in Ca+ influx seemed to sustain the mechanical response. This was because D600 (a calcium influx blocker) failed to completely relax K+-induced contraction in the absence of Na+ and also because the ability of EGTA to produce relaxation was reduced in the absence of Na+. Measurement of tissue calcium content using the lanthanum method revealed coincident decrease in tissue calcium and tension to control level during Na+-mediated relaxation. The results suggest a role for transmembrane Na+-Ca++ exchange in causing the Na+-mediated relaxation of taenia undergoing Na+-free contracture.
当培养基中不存在钠离子时,高钾引起的豚鼠结肠带收缩经冲洗后无法逆转。重新加入钠离子(7 mM或更高)会导致舒张。大鼠子宫也得到了类似结果。钠替代的作用并非由于离子强度的改变,因为等摩尔或更高摩尔数的胆碱、钙离子、钾离子、锰离子或镁离子几乎没有作用。在无钠培养基中收缩的持续并非由于收缩装置的“捕捉状态”。细胞质中钙离子移除受损而非钙离子内流持续增加似乎维持了机械反应。这是因为在无钠情况下,D600(一种钙离子内流阻滞剂)未能完全舒张钾离子诱导的收缩,还因为在无钠情况下,EGTA产生舒张的能力降低。使用镧法测量组织钙含量显示,在钠离子介导的舒张过程中,组织钙含量和张力同时下降至对照水平。结果表明,跨膜钠钙交换在导致无钠挛缩的结肠带钠离子介导的舒张中起作用。