Nasu Y, Sakamoto Y
Department of Physiology, School of Medicine, Fukuoka University, Japan.
Nihon Heikatsukin Gakkai Zasshi. 1990 Aug;26(4):191-8. doi: 10.1540/jsmr1965.26.191.
Verapamil (10(-6) M) significantly reduced a development of the membrane depolarization and the contracture which were induced by Na removal. The fully developed depolarization, after exposure to Na-free solution, was reduced greatly by verapamil, excess Ca (15 mM) or sodium nitroprusside (10(-6) M), but some depolarization still remained. This remaining depolarization was completely blocked by readmission of 10 mM Na to Na-free solution containing verapamil, excess Ca or sodium nitroprusside. However, Mn (1.5 mM) did not block the depolarization due to Na removal and if Mn was present in Na-free solution, readmission of 15 mM Na to Na-free solution was not able to block the depolarization. On the other hand, the contracture due to Na removal was inhibited by addition of Mn (1.5 mM) or sodium nitroprusside (10(-6) M), but partially by addition of verapamil (10(-6) M) or excess Ca, to Na-free solution. These remaining contractures were also abolished by readmission of 10 mM Na to Na-free solution containing verapamil or excess Ca. Thus, these results suggest that the depolarization and the contracture due to Na removal are induced by increase in cytoplasmic Ca concentrations through (1): verapamil-sensitive Ca channel, (2): Na-Ca exchange system and (3): some mechanism which is inhibited by sodium nitroprusside.
维拉帕米（10⁻⁶ M）能显著减轻因去除钠离子而诱导产生的膜去极化和挛缩。在暴露于无钠溶液后，完全发展的去极化被维拉帕米、过量的钙（15 mM）或硝普钠（10⁻⁶ M）大幅降低，但仍有一些去极化存在。通过向含有维拉帕米、过量钙或硝普钠的无钠溶液中重新加入10 mM钠离子，这种剩余的去极化被完全阻断。然而，锰（1.5 mM）并不能阻断因去除钠离子而产生的去极化，并且如果在无钠溶液中存在锰，向无钠溶液中重新加入15 mM钠离子并不能阻断去极化。另一方面，因去除钠离子而产生的挛缩可被加入锰（1.5 mM）或硝普钠（10⁻⁶ M）抑制，但向无钠溶液中加入维拉帕米（10⁻⁶ M）或过量钙只能部分抑制。通过向含有维拉帕米或过量钙的无钠溶液中重新加入10 mM钠离子，这些剩余的挛缩也被消除。因此，这些结果表明，因去除钠离子而产生的去极化和挛缩是通过以下途径由细胞质钙浓度升高诱导产生的：（1）维拉帕米敏感的钙通道；（2）钠钙交换系统；（3）某种被硝普钠抑制的机制。
