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LOSS OF CHOLINERGIC POTENTIATING RESPONSIVENESS IN MOUSE ISLETS TRANSPLANTED TO THE KIDNEY

Pancreatic islets from BALB/c mice were transplanted to the kidney of syngeneic hosts. After 1–40 weeks, the grafts were removed, perifused in vitro, and extracted. Fresh islets were similarly examined. The graft insulin content fell by 70% in 1 week and remained low throughout the observation period. In contrast, rates of basal or glucose-stimulated insulin release were not much, if at all, decreased. In fresh islets and grafts removed after 3 or 28 weeks, 2 consecutive pulses of glucose stimulation, 20–25 min long and separated by 20 min at basal glucose concentration (2 or 2.8 mmol/L), elicited the same insulin secretory response. When 10 μmol/L acetylcholine and 10 μmol/L eserine were present during the second pulse, the glucose-stimulated insulin release from fresh islets was potentiated as much as 11-fold. This potentiation was reduced by one half during the first week of transplantation, and subsequently by 80–90%. It is concluded that vagal deprivation rapidly induces a state of persistent cholinergic refractoriness in transplanted β-cells, despite morphological signs of autonomic reinnervation of the grafts.