EFFECTS OF ACUTE SODIUM OMISSION ON INSULIN RELEASE, IONIC FLUX AND MEMBRANE-POTENTIAL IN MOUSE PANCREATIC B-CELLS
EFFECTS OF ACUTE SODIUM OMISSION ON INSULIN RELEASE, IONIC FLUX AND MEMBRANE-POTENTIAL IN MOUSE PANCREATIC B-CELLS
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DOI：
10.1016/0167-4889(88)90076-6
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发表时间：
1988-04-25
期刊：
影响因子：
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通讯作者：
HENQUIN, JC
中科院分区：
文献类型：
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作者：
DEMIGUEL, R;TAMAGAWA, T;HENQUIN, JC
用胆碱和锂盐分别作为非替代和非替代，在小鼠胰岛上研究了细胞外Na+的急性缺失对胰岛B细胞功能的影响。在无葡萄糖条件下，胆碱替代Na+使B细胞膜超极化，抑制86Rb+和45Ca+外流，但不影响胰岛素的释放。相反，Li+替代Na+使B细胞膜去极化，并引起非钙依赖的45Ca~(2+)外流和胰岛素释放的瞬时加速。在10 mM葡萄糖和2.5 mM Ca~(2+)存在下，胆碱替代Na+再次使B细胞膜迅速超极化。这种超极化之后是一个持续的尖峰活动的去极化阶段，然后膜电位的长慢波恢复。在此条件下，86Rb+外流先下降后加速，45Ca+外流和胰岛素释放显著平行增加。在无Ca~(2+)条件下，胆碱替代Na~(2+)可抑制45Ca~(2+)和86Rb~+外流，对胰岛素释放无影响。在10 mM葡萄糖存在下，Na+被Li+置换，使B细胞膜迅速去极化，引起强烈的持续尖峰活动，并加速45Ca+外流、86Rb+外流和胰岛素释放。在无细胞外Ca~(2+)的情况下，Li~(2+)仍可引起45Ca~(2+)、86Rb~(+)外流和胰岛素释放的快速而短暂的增加。虽然Na+不是胰岛素释放所必需的，但它通过调节B细胞的膜电位和离子通量等，在刺激-分泌偶联过程中发挥着重要的调节作用。
The effects of acute omission of extracellular Na+on pancreatic B-cell function were studied in mouse islets, using choline and lithium salts as impermeant and permeant substitutes, respectively. In the absence of glucose, choline substitution for Na+hyperpolarized the B-cell membrane, inhibited86Rb+and45Ca2+efflux, but did not affect insulin release. In contrast, Li+substitution for Na+depolarized the B-cell membrane and caused a Ca2+-independent, transient acceleration of45Ca2+efflux and insulin release. Na+replacement by choline in the presence of 10 mM glucose and 2.5 mM Ca2+again rapidly hyperpolarized the B-cell membrane. This hyperpolarization was then followed by a phase of depolarization with continuous spike activity, before long slow waves of the membrane potential resumed. Under these conditions,86Rb+efflux first decreased before accelerating, concomitantly with marked and parallel increases in45Ca2+efflux and insulin release. In the absence of Ca2+,45Ca2+and86Rb+efflux were inhibited and insulin release was unaffected by choline substitution for Na+. Na+replacement by Li+in the presence of 10 mM glucose rapidly depolarized the B-cell membrane, caused an intense continuous spike activity, and accelerated45Ca2+efflux,86Rb+efflux and insulin release. In the absence of extracellular Ca2+, Li+still caused a rapid but transient increase in45Ca2+and86Rb+efflux and in insulin release. Although not indispensable for insulin release, Na+plays an important regulatory role in stimulus-secretion coupling by modulating, among others, membrane potential and ionic fluxes in B-cells.