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胰岛素对大鼠比目鱼肌中钠和钾转运的影响。

The effect of insulin on the transport of sodium and potassium in rat soleus muscle.

作者信息

Clausen T, Kohn P G

出版信息

J Physiol. 1977 Feb;265(1):19-42. doi: 10.1113/jphysiol.1977.sp011703.

Abstract
  1. The action of insulin on the transport and the distribution of Na and K has been studied in rat soleus muscles incubated at 30 degrees C in glucose-free Krebs-Ringer bicarbonate buffer. 2. Measurements of the uptake and the wash-out of 22Na indicate that the muscles contain an intracellular pool of Na available for transport which is confined to the water space not available to sucrose. Ouabain (10(-4)-10(-3)M) inhibited 22Na efflux by 69% (0-287 micronmole/g tissue wet weight per minute) and 42K-influx by 40% (0-196 micronmole/g tissue wet weight per minute). When all extracellular Na was replaced by Li, both 22Na-efflux adn 42K-influx were inhibited to about the same extent and ouabain produced very little further inhibition. 2,4-dinitrophenol decreased the ouabain-resistant component of 22Na-efflux by 39%. 3. Insulin (from 0-1 to 100 mu./ml.) increased the rate coefficient of 22Na-efflux by from 11 to 46% within 15 min. In the presence of ouabain (10(-3)M), the same relative increase was obtained, indicating that the hormone stimulates the glycoside-sensitive and the glycoside-insensitive Na transport to a similar extent. The effect of insulin on 22Na-efflux was not abolished by tetracaine (0-5 X 10(-3)M), phlorizin (0-5 X 10(-2)M) or by the substitution of Na, K, Mg or Ca. In the presence of 2,4-dinitrophenol (0-5 X 10(-4)M) or at temperatures below 15 degrees C, the hormone produced no detectable change in 22Na-efflux. 4. Insulin increased 42K-influx from 0-525 to 0-664 mumole/g tissue wet weight per minute. This effect was entirely blocked by ouabain but not by tetracaine. Insulin produced a 14% transient decrease in 42K-efflux. 5. The continued exposure to insulin led to a new steady state, in which the intracellular Na pool was decreased from around 10 to around 5 mumole/g tissue wet weight and the K content increased by an equivalent amount. In the presence of ouabain or at low extracellular concentrations of K, insulin increased the rate of 22Na-influx by around 35%. This effect was blocked by 2,4-dinitrophenol but not be tetracaine. 6. It is concluded that insulin stimulates the active coupled transport of Na and K, possibly by increasing the relative Na-affinity of the system mediating this process.
摘要
  1. 在30℃下于无糖的 Krebs - Ringer 碳酸氢盐缓冲液中孵育的大鼠比目鱼肌中,研究了胰岛素对钠和钾的转运及分布的作用。2. 对22Na摄取和洗脱的测量表明,肌肉中存在一个可供转运的细胞内钠池,该钠池局限于蔗糖无法进入的水空间。哇巴因(10(-4)-10(-3)M)抑制22Na外流69%(0 - 287微摩尔/克组织湿重每分钟),抑制42K内流40%(0 - 196微摩尔/克组织湿重每分钟)。当所有细胞外钠被锂取代时,22Na外流和42K内流均受到大致相同程度的抑制,哇巴因几乎不再产生进一步抑制作用。2,4 - 二硝基苯酚使22Na外流的哇巴因抗性成分降低39%。3. 胰岛素(0 - 1至100微单位/毫升)在15分钟内使22Na外流的速率系数增加11%至46%。在哇巴因(10(-3)M)存在的情况下,获得了相同的相对增加,表明该激素对糖苷敏感和糖苷不敏感的钠转运的刺激程度相似。胰岛素对22Na外流的作用未被丁卡因(0 - 5×10(-3)M)、根皮苷(0 - 5×10(-2)M)或钠、钾、镁或钙的替代所消除。在2,4 - 二硝基苯酚(0 - 5×10(-4)M)存在的情况下或在低于15℃的温度下,该激素未使22Na外流产生可检测到的变化。4. 胰岛素使42K内流从0 - 525增加至0 - 664微摩尔/克组织湿重每分钟。此作用完全被哇巴因阻断,但未被丁卡因阻断。胰岛素使42K外流短暂降低14%。5. 持续暴露于胰岛素导致一种新的稳态,其中细胞内钠池从约10微摩尔/克组织湿重降至约5微摩尔/克组织湿重,钾含量等量增加。在哇巴因存在或细胞外钾浓度较低时,胰岛素使22Na内流速率增加约35%。此作用被2,4 - 二硝基苯酚阻断,但未被丁卡因阻断。6. 得出结论,胰岛素可能通过增加介导此过程的系统的相对钠亲和力来刺激钠和钾的主动偶联转运。

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