Somatostatin- and Epinephrine-Induced Modifications of 45Ca++ Fluxes and Insulin Release in Rat Pancreatic Islets Maintained in Tissue Culture

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Abstract
The effects of somatostatin and epinephrine have been studied with regard to glucose-induced insulin release and 45Ca++ uptake by rat pancreatic islets after 2 days in tissue culture and with regard to 45Ca++ efflux from islets loaded with the radio-isotope during the 2 days of culture. 45Ca++ uptake, measured simultaneously with insulin release, was linear with time for 5 min. 45Ca++ efflux and insulin release were also measured simultaneously from perifused islets. Glucose (16.7 mM) markedly stimulated insulin release and 45Ca++ uptake. Somatostatin inhibited the stimulation of insulin release by glucose in a concentration-related manner (1-1,000 ng/ml) but was without effect on the glucose-induced stimulation of 45Ca++ uptake. Similarly, under perifusion conditions, both phases of insulin release were inhibited by somatostatin while no effect was observed on the pattern of 45Ca++ efflux after glucose. Epinephrine, in contrast to somatostatin, caused a concentration-dependent inhibition of the stimulation of both insulin release and 45Ca++ uptake by glucose. Both phases of insulin release were inhibited by epinephrine and marked inhibition could be observed with no change in the characteristic glucose-evoked pattern of 45Ca++ efflux (e.g., with 10 nM epinephrine). The inhibitory effect of epinephrine on 45Ca++ uptake and insulin release appeared to be mediated via an α-adrenergic mechanism, since is was abolished in the presence of phentolamine. Somatostatin inhibits insulin release without any detectable effect upon the handling of calcium by the islets. In contrast, inhibition of insulin release by epinephrine is accompanied by a partial inhibition of glucose-induced Ca++ uptake.