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豚鼠输尿管中钠钙交换的证据。

Evidence for sodium-calcium exchange in the guinea-pig ureter.

作者信息

Aickin C C, Brading A F, Burdyga T V

出版信息

J Physiol. 1984 Feb;347:411-30. doi: 10.1113/jphysiol.1984.sp015073.

Abstract

The effects of high-K and low-Na solutions on the smooth muscle of the guinea-pig ureter have been examined in both normal tissues, and tissues in which the Na pump had been blocked by exposure to K-free solutions or ouabain (high-Na tissues). Tension recording, membrane potential measurements and ion analysis were used. High-K solutions depolarize normal tissues, leading to action potential generation and phasic contractions followed, at concentrations greater than 20-30 mM, by cessation of action potentials and the development of a biphasic contracture which declines slowly during continuous exposure. The contracture is abolished by Ca-antagonist drugs, procaine and Ca-free solutions. Short exposures of normal tissues to Na-free solutions do not result in tension development. Longer exposures may initiate tension, depending on the Na substitute used. Sucrose causes depolarization of the cells and spike development associated with phasic contractions, superimposed on a small contracture; Li depolarizes the cells but causes no tension generation; Tris hyperpolarizes the cells and a small increase in basal tone may be seen. On exposure to K-free solutions or ouabain, the tissues do not develop significant tone but their response to short application of high-K solutions grows with time. The tissues also develop the ability to contract on short applications of low-Na solutions. The low-Na contractures are resistant to concentrations of Ca antagonists that abolish the K responses of normal tissues, but are abolished in Ca-free solutions. The ability of the tissues to contract in Na-free solutions is accompanied by an increase in intracellular Na and loss of intracellular K. Even after several hours' exposure to ouabain, however, the tissues still contain significant amounts of K and the membrane potential is the same as, or more negative than that in normal tissues. Therefore it appears that another mechanism, apart from the Na pump, can regulate intracellular Na. On continuous exposure to Na-free solutions, the contracture declines rapidly. The decline is associated with a loss of intracellular Na. The Na-free contracture is larger when K rather than Tris is used as the substitute. This difference persists in the presence of a concentration of Mn that abolishes the K contracture of normal tissues but is abolished by high concentrations (10 mM) of procaine.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

已在正常组织以及通过暴露于无钾溶液或哇巴因(高钠组织)使钠泵被阻断的组织中,研究了高钾和低钠溶液对豚鼠输尿管平滑肌的影响。采用张力记录、膜电位测量和离子分析方法。高钾溶液使正常组织去极化,导致动作电位产生和相性收缩,在浓度大于20 - 30 mM时,随后动作电位停止,并出现双相挛缩,在持续暴露期间缓慢下降。该挛缩可被钙拮抗剂药物、普鲁卡因和无钙溶液消除。正常组织短期暴露于无钠溶液不会导致张力产生。较长时间暴露可能会引发张力,这取决于所使用的钠替代物。蔗糖导致细胞去极化和与相性收缩相关的锋电位产生,叠加在小的挛缩之上;锂使细胞去极化但不产生张力;三羟甲基氨基甲烷使细胞超极化,可观察到基础张力略有增加。暴露于无钾溶液或哇巴因时,组织不会产生明显张力,但它们对短期应用高钾溶液的反应会随时间增加。组织在短期应用低钠溶液时也会产生收缩能力。低钠挛缩对能消除正常组织钾反应的钙拮抗剂浓度具有抗性,但在无钙溶液中会被消除。组织在无钠溶液中收缩的能力伴随着细胞内钠增加和细胞内钾丢失。然而,即使在暴露于哇巴因数小时后,组织仍含有大量钾,且膜电位与正常组织相同或更负。因此,似乎除了钠泵之外,还有另一种机制可以调节细胞内钠。持续暴露于无钠溶液时,挛缩迅速下降。这种下降与细胞内钠的丢失有关。当用钾而非三羟甲基氨基甲烷作为替代物时,无钠挛缩更大。在存在能消除正常组织钾挛缩但被高浓度(10 mM)普鲁卡因消除的锰浓度时,这种差异仍然存在。(摘要截取自400字)

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