EFFECTS OF INTRACELLULAR ADENOSINE-5'-DIPHOSPHATE AND ORTHOPHOSPHATE ON SENSITIVITY OF SODIUM EFFLUX FROM SQUID AXON TO EXTERNAL SODIUM AND POTASSIUM
EFFECTS OF INTRACELLULAR ADENOSINE-5'-DIPHOSPHATE AND ORTHOPHOSPHATE ON SENSITIVITY OF SODIUM EFFLUX FROM SQUID AXON TO EXTERNAL SODIUM AND POTASSIUM
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DOI：
10.1085/jgp.56.5.583
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发表时间：
1970-01-01
影响因子：
3.8
通讯作者：
DEWEER, P
中科院分区：
文献类型：
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作者：
DEWEER, P
研究了鱿鱼巨轴突的钠外排及其对外部钾和钠的敏感性。当未处理的轴突流出的钠被Ko强烈刺激时，naoh被抑制；当对Kowas low的依赖时，nao具有刺激作用。早期CN中毒或apyrase注射可产生高水平的细胞内adp1和Pi，使钠外排对外部K的依赖减少，而对外部Na的依赖增加。注射ADP、AMP、精氨酸或肌酸+肌酸磷酸激酶均能提高ADP水平，但不升高pilins水平，其效果与早期CN中毒相同。针剂注射对钠外排钾敏感性无影响。当ATP:ADP比值降低时，被精氨酸酶耗尽的轴突仍丧失其K敏感性，当该比值升高时部分恢复。粗略计算表明，当ATP:ADP比约为10:1时，钠外排对ko的依赖性最大，当ATP:ADP比约为1:2时，钠外排对ko不敏感，当ATP:ADP比约为1:10时，钠外排受到ko的抑制。当注入完整的轴突时，脱氧atp模拟ADP。过量的Mg和Pi抑制了对虾黄素敏感和对虾黄素不敏感的钠流出。提出了一个可以解释ADP、pii和脱氧atp作用的模型。
A study was made of sodium efflux from squid giant axon, and its sensitivity to external K and Na. When sodium efflux from untreated axons was strongly stimulated by Ko, Naowas inhibitory; when dependence on Kowas low, Naohad a stimulatory effect. Incipient CN poisoning or apyrase injection, which produces high intracellular levels of ADP1and Pi, rendered sodium efflux less dependent on external K and more dependent on external Na. Injection of ADP, AMP, arginine, or creatine + creatine phosphokinase, all of which raise ADP levels without raising Pilevels, had the same effect as incipient CN poisoning. Piinjection had no effect on the K sensitivity of sodium efflux. Axons depleted of arginine and phosphoarginine by injection of arginase still lost their K sensitivity when the ATP:ADP ratio was lowered and regained it partially when the ratio was raised. Rough calculations show that sodium efflux is maximally Ko-dependent when the ATP:ADP ratio is about 10:1, becomes insensitive to Kowhen the ratio is about 1:2, and isinhibitedby Kowhen the ratio is about 1:10. Deoxy-ATP mimicked ADP when injected into intact axons. Excess Mg, as well as Pi, inhibited both strophanthidin-sensitive and strophanthidin-insensitive sodium efflux. An outline is presented for a model which might explain the effects of ADP, Piand deoxy-ATP.