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.
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