Somers G, Devis G, van Obberghen E, Malaisse W J
Pflugers Arch. 1976 Sep 3;365(1):21-8. doi: 10.1007/BF00583624.
The modality of Ba2+-induced insulin release was investigated in the isolated perfused rat pancreas. The insulinotropic action of Ba2+ was antagonized by Ca2+, Mg2+ and verapamil, and enhanced by EGTA, theophylline, glucose and cytochalasin B. Likewise the net uptake of 133Ba2+ by isolated islets was inhibited by Ca2+, Mg2+ and verapamil. Glucose increased 133Ba2+ net uptake, but only when sufficient Ba2+ had accumulated in the islets. Theophylline failed to affect 133Ba2+ net uptake. These data suggest that (i) Ba2+-induced insulin release is dependent on the accumulation of this cation in the B-cell; (ii) Ba2+ inward transport in the B-cell occurs through a verapamil-sensitive channel characterized by competition between Ba2+, Ca2+ and Mg2+; and (iii) the enhancing effect of theophylline upon insulin release could be due to an intracellular translocation of alkaline-earth cations rather than to an increase in their net uptake. The present findings also support the idea that insulin release can be triggered by the accumulation of suitable divalent cations in a critical site of the B-cell, leading to the activation of a cytochalasin B-response effector system.
在离体灌注大鼠胰腺中研究了Ba2+诱导胰岛素释放的方式。Ba2+的促胰岛素作用被Ca2+、Mg2+和维拉帕米拮抗，而被EGTA、茶碱、葡萄糖和细胞松弛素B增强。同样，Ca2+、Mg2+和维拉帕米抑制了分离胰岛对133Ba2+的净摄取。葡萄糖增加了133Ba2+的净摄取，但仅当胰岛中积累了足够的Ba2+时才会如此。茶碱未能影响133Ba2+的净摄取。这些数据表明：（i）Ba2+诱导的胰岛素释放依赖于该阳离子在B细胞中的积累；（ii）B细胞中Ba2+的内向转运通过一个对维拉帕米敏感的通道进行，其特征为Ba2+、Ca2+和Mg2+之间存在竞争；（iii）茶碱对胰岛素释放的增强作用可能是由于碱土金属阳离子的细胞内转运，而非其净摄取增加。本研究结果还支持以下观点，即胰岛素释放可由合适的二价阳离子在B细胞关键位点的积累触发，从而导致细胞松弛素B反应效应系统的激活。
