Article révisé par les pairs
Résumé : The effect of Na+ deprivation upon the kinetics of immunoreactive insulin (IRI) secretion was studied in perfused rat islets of Langerhans. Partial replacement of Na+ by choline (24 mM Na+, 119 mM choline) did not modify either phase of glucose induced (300 mg/100 ml) IRI release. Total replacement of Na+ by choline in a low glucose (50 mg/100 ml) medium provoked a rapid secretory phase, unaffected by the presence of atropine (2.5 μg/ml). When Na+ withdrawal coincided with glucose stimulation, the first secretory phase was not significantly affected, whereas the second phase was inhibited progressively with time. In a medium depleted of Na+ for 25 min before glucose stimulation, the sugar induced only a diminished first phase but no second phase. This inhibitory effect was reversible approximately 5 min after restoration of a normal Na+ concentration in the perfusate. Total replacement of Na+ by Li+ and choline (118 mM Li+, 24 mM choline) also elicited a small increase in basal secretion rate. When Na+ was partially replaced by Li+ (24 mM Na+, 119 mM Li+) at the time of increasing glucose concentration, the first phase was decreased and the second phase was markedly inhibited. Both secretory phases were completely obliterated when glucose stimulation was applied 25 min after partial replacement of Na+ by Li+. This inhibition was poorly reversible. These data indicate that extracellular Na+ is required for both phases of glucose induced IRI release. They support the concept that the concentration of Na+ in the beta cell is of critical importance in the secretory process. (31 references)