Carpinelli A R, Malaisse W J
Diabete Metab. 1980 Sep;6(3):193-8.
The fractional outflow rate (FOR) of 86 Rb from prelabelled and perifused rat pancreatic islets increased in response to either extracellular acidosis (which causes intracellular acidification) or extracellular alkalosis (which increases the pH gradient across the plasma membrane). However, when the extracellula pH was maintained at 7.4 and ths islet cells acidified by exposure to a high pCO2, a modest decrease in 86 Rb FOR was observed. This decrease was followed by a secondary and transient increased in 86 Rb FOR. The secondary increase was more marked in the presence than absence of glucose, and, in the former case, was unaffected by tetraethylammonium or quinine, suggesting that it may be due to an intracellular redistribution of 86 Rb. Glucose markedly inhibited 86 Rb FOR whether at normal or high pCO2. It is concluded that an increase in H+ generation rate only plays a minor role, if any, in the inhibitory effect of glucose on 86 Rb FOR.
预先标记并进行灌流的大鼠胰岛中86Rb的分数流出率（FOR），会因细胞外酸中毒（导致细胞内酸化）或细胞外碱中毒（增加跨质膜的pH梯度）而升高。然而，当细胞外pH维持在7.4，且胰岛细胞因暴露于高pCO2而酸化时，观察到86Rb FOR有适度下降。这种下降之后是86Rb FOR的二次短暂升高。在有葡萄糖存在的情况下，二次升高比没有葡萄糖时更明显，并且在前一种情况下，不受四乙铵或奎宁的影响，这表明它可能是由于86Rb在细胞内的重新分布。无论在正常还是高pCO2条件下，葡萄糖都能显著抑制86Rb FOR。得出的结论是，H+生成速率的增加在葡萄糖对86Rb FOR的抑制作用中，即使有作用也只起次要作用。
