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The effects of the mixed /β-agonist adrenaline on insulin secretion from isolated human islets of Langerhans were studied. In static incubation experiments, adrenaline (0·1 nmol/l to 10 µmol/l) caused a concentration-dependent inhibition of glucose-induced insulin secretion from isolated human islets. However, perifusion experiments revealed that the time-course of the secretory changes induced by adrenaline was complex. When employed at a high concentration (1 µmol/l), adrenaline caused a sustained inhibition of glucose-induced insulin secretion, which could be relieved by the addition of the ₂-antagonist yohimbine (10 µmol/l). By contrast, infusion of adrenaline at a lower concentration (10 nmol/l), produced a large initial potentiation of glucose-induced insulin secretion. This response was, however, short-lived and followed by sustained inhibition of secretion, which could be relieved by yohimbine (10 µmol/l). The initial stimulation of insulin secretion provoked by 10 nmol adrenaline/l was abolished when islets were incubated in the presence of the β-antagonist, propranolol (1 µmol/l), consistent with activation of β-adrenoceptors. In support of this, treatment of human islets with the selective β₂-agonist clenbuterol, was also associated with marked stimulation of insulin secretion. By contrast, each of two selective β₃-agonists tested failed to alter insulin secretion from human islets. The results indicate that human pancreatic B-cells are equipped with both ₂-and β₂-adrenoceptors which can affect insulin secretion. Adrenaline interacts with both of these but the ₂-response is predominant and can overcome the tendency of β₂-adrenoceptors to potentiate insulin release.

Journal of Endocrinology (1993) 138, 555–563

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