Article révisé par les pairs
Résumé : The fractional outflow rate (FOR) of 86Rb from prelabelled and perifused rat pancreatic islets increased in response to either extracellular acidosis (which causes intracellular acidification) or extracellular alkalosis (which increased the pH gradient across the plasma membrane). However, when the extracellular pH was maintained at 7.4 and the islet cells acidified by exposure to a high pCO2, a modest decrease in 86Rb FOR was observed. This decrease was followed by a secondary and transient increase in 86Rb 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 86Rb. Glucose markedly inhibited 86Rb 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 86Rb FOR.