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肾上腺素诱导的钾离子外流导致交感神经节中钠泵的刺激。

Adrenaline-induced K+ efflux results in sodium pump stimulation in a sympathetic ganglion.

作者信息

Smith P A, Thompson E L, Zidichouski J A

出版信息

Neurosci Lett. 1986 Oct 30;71(1):72-6. doi: 10.1016/0304-3940(86)90259-4.

Abstract

The potassium-activated hyperpolarization (KH) was used as an index of electrogenic Na+ pumping in bullfrog sympathetic ganglia. This response was evoked by storing ganglia in K-free Ringer's solution and briefly introducing normal Ringer's solution containing 2 mM K+ at regular intervals. The apparent EC50 for K+ was 2.21 mM (range 0.88-3.54 mM, for n = 5) and at least 10 mM K+ was required to produce a maximal KH response. Adrenaline, which produces membrane hyperpolarization by increasing K+ conductance (gK), increased the amplitude of KH responses. When the K+ efflux accompanying the adrenaline-induced hyperpolarization (AdH) was blocked with 2 mM Ba2+, the KH was no longer potentiated. It is suggested that the K+ moving out of the cells during the AdH accumulates extracellularly and stimulates the Na+ pump.

摘要

钾激活超极化(KH)被用作牛蛙交感神经节中电生性钠泵的指标。通过将神经节储存在无钾林格氏液中,并定期短暂引入含2 mM钾的正常林格氏液来诱发这种反应。钾的表观半数有效浓度(EC50)为2.21 mM(n = 5时范围为0.88 - 3.54 mM),至少需要10 mM钾才能产生最大的KH反应。肾上腺素通过增加钾电导(gK)产生膜超极化,增加了KH反应的幅度。当用2 mM Ba2+阻断伴随肾上腺素诱导超极化(AdH)的钾外流时,KH不再增强。提示在AdH期间从细胞中移出的钾在细胞外积累并刺激钠泵。

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