Maggi C A, Meli A
Experientia. 1984 Jul 15;40(7):681-6. doi: 10.1007/BF01949721.
Addition of KC1 (40 mM) produced rhythmic contractions of guinea-pig ureters in vitro which were unaffected by phentolamine, atropine or tetrodotoxin. KC1 failed to elicit rhythmic contractions of ureters incubated in a Krebs solution with no added Ca++; in these conditions the addition of CaC12 in concentrations of 1.5 mM, or higher, produced rhythmic contractions whose frequency, but not amplitude, was proportional to CaC12 concentration in the bathing medium. EDTA reduced the frequency of KC1-induced rhythmic contractions without affecting their amplitude. Nifedipine and verapamil reduced both the frequency and the amplitude of KC1-induced rhythmic contraction; verapamil was more effective than nifedipine in reducing their amplitude. Urethane reduced the amplitude without significantly affecting the frequency of KC1-induced rhythmic contractions. An increase in the extracellular Ca++ concentration reverted the suppressive effect of all drugs under study. These results suggest that an influx of Ca++ from the extracellular space is responsible for the initiation of KC1-induced rhythmic contractions and is involved in the mechanism(s) which regulates their frequency, but that a separate mechanism regulates their amplitude.
加入氯化钾（40 mM）可使豚鼠输尿管在体外产生节律性收缩，这种收缩不受酚妥拉明、阿托品或河豚毒素的影响。在不添加钙离子的 Krebs 溶液中孵育的输尿管，氯化钾无法引发节律性收缩；在这些条件下，添加浓度为 1.5 mM 或更高的氯化钙可产生节律性收缩，其频率与浴液中氯化钙浓度成正比，但振幅不变。乙二胺四乙酸降低了氯化钾诱导的节律性收缩的频率，但不影响其振幅。硝苯地平和维拉帕米降低了氯化钾诱导的节律性收缩的频率和振幅；维拉帕米在降低振幅方面比硝苯地平更有效。乌拉坦降低了振幅，但对氯化钾诱导的节律性收缩的频率没有显著影响。细胞外钙离子浓度的增加可逆转所有研究药物的抑制作用。这些结果表明，细胞外空间钙离子的内流是氯化钾诱导的节律性收缩起始的原因，并且参与调节其频率的机制，但存在一个单独的机制调节其振幅。
