Stout M A, Diecke F P, Greenberg S
Arch Int Pharmacodyn Ther. 1980 Feb;243(2):292-303.
The effects of metabolic inhibitors on ATP levels and on 45Ca fluxes were studied in desheathed tibial nerves of Rana pipiens. ATP levels were significantly reduced and Ca influx and efflux increased following exposure to cyanide, mersalyl, azide, dinitrophenol, iodoacetate or ethacrynic acid. The efflux changes were relatively small compared to squid axons but are not attributable to depolarization of the cell or to changes in the transmembrane Na gradient. The magnitude of the effluxes are consistent with ideas about the amount of labile Ca sequestered in energy-dependent Ca pools. The efflux stimulated by metabolic inhibitors is reduced by removing extracellular Na or Ca, indicating that a large portion of Ca efflux in the poisoned state is mediated by Na-Ca countertransport. In the nominal absence of both these cations Ca efflux can be stimulated by metabolic inhibitors, suggesting that mechanisms in addition to countertransport participate in Ca efflux.
在牛蛙去鞘胫神经中研究了代谢抑制剂对ATP水平和45Ca通量的影响。暴露于氰化物、汞撒利、叠氮化物、二硝基苯酚、碘乙酸或依他尼酸后,ATP水平显著降低,钙内流和外流增加。与乌贼轴突相比,外流变化相对较小,但这并非归因于细胞去极化或跨膜钠梯度的变化。外流的幅度与关于能量依赖钙库中不稳定钙含量的观点一致。去除细胞外钠或钙可减少代谢抑制剂刺激的外流,表明在中毒状态下大部分钙外流是由钠-钙逆向转运介导的。在名义上同时缺乏这两种阳离子的情况下,代谢抑制剂仍可刺激钙外流,这表明除逆向转运外的其他机制也参与了钙外流。