Sunano S
Jpn J Pharmacol. 1984 Jan;34(1):51-6. doi: 10.1254/jjp.34.51.
Lowering of temperature applied during the course of the tonic contraction of high-K-induced contracture of guinea-pig vas deferens induced an increase in tension which was sensitive to extracellular Ca. Verapamil and nifedipine inhibited the tonic contraction and cooling-induced tension development. Mn2+ and La3+ also showed inhibiting actions on the tonic contraction, which, however, was followed by slow re-elevation of the tension. Cooling treatment caused relaxation in the presence of either ion, which increased with repetition of the cooling treatment. By rewarming the preparation, a phasic contraction, which increased in height with repetition of the treatment, was observed. These effects in the presence of Mn2+ or La3+ were also observed in the absence of Ca or in preparations treated with caffeine in Ca-free solution (Ca-deprived preparation). Verapamil was capable of depressing these effects of Mn2+ and La3+. These results suggest the involvement of influxed Ca in the initiation of tension development by cooling. The decrease of extrusion through the cell membrane and/or uptake by intracellular binding sites at low temperature may be the cause of the cooling-induced tension development. Mn2+ or La3+ induces the tension development by their direct actions on contractile proteins which are differently affected by the changes in temperature.
在豚鼠输精管高钾诱导的强直性收缩过程中施加降温，会引起张力增加，这种增加对细胞外钙敏感。维拉帕米和硝苯地平抑制强直性收缩以及降温诱导的张力发展。锰离子和镧离子也对强直性收缩有抑制作用，然而，随后张力会缓慢回升。在任一离子存在的情况下，降温处理都会引起舒张，且随着降温处理的重复而增强。通过对标本复温，可观察到一种相性收缩，其幅度随着处理的重复而增加。在无钙或在无钙溶液中用咖啡因处理的标本（缺钙标本）中，在锰离子或镧离子存在的情况下也观察到了这些效应。维拉帕米能够抑制锰离子和镧离子的这些效应。这些结果表明，降温诱导张力发展的起始过程中有内流钙的参与。低温时通过细胞膜的外排减少和/或细胞内结合位点摄取减少可能是降温诱导张力发展的原因。锰离子或镧离子通过其对收缩蛋白的直接作用诱导张力发展，而收缩蛋白受温度变化的影响不同。
