Effects of α‐ and β‐adrenoceptor stimulation on 45Ca2+ efflux and insulin secretion from perfused rat islets

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Abstract
Exposure to the beta 2-adrenoceptor agonist terbutaline resulted in a transient stimulation of 45Ca2+ efflux from 45Ca2+ preloaded rat islets perfused in 2 mM Ca2+ and 8.3 mM glucose. Concomitantly, an increase in insulin secretion occurred. Under the same experimental conditions, the alpha-adrenoceptor agonist noradrenaline promptly inhibited insulin release without any apparent influence on 45Ca2+ efflux. In contrast, in a medium containing 2 mM Ca2+ and a low glucose concentration (2.8 mM), terbutaline stimulated insulin secretion without any apparent effects on 45Ca2+ efflux. Noradrenaline had no effect on insulin secretion or 45Ca2+ efflux in this medium. When islets were perfused with 8.3 mM glucose in a Ca2+ deficient medium, with or without addition of the chelating agent EGTA, terbutaline induced a marginal stimulation of insulin secretion and a negligible stimulation of 45Ca2+ efflux. On the contrary, noradrenaline stimulated to an immediate and notable 45Ca2+ efflux in these Ca2+ deficient media. Noradrenaline also clearly inhibited insulin secretion, though less markedly and with a slower onset than in islets perfused in 2 mM Ca2+. When the islets were perfused in a Ca2+ deficient medium with 2.8 mM glucose, terbutaline had a slight insulin releasing effect, but stimulated 45Ca2+ efflux potently. Noradrenaline had no influence on insulin secretion but a weak stimulatory effect on 45Ca2+ efflux. The data suggest that the beta 2-adrenoceptor agonist terbutaline has the ability to stimulate insulin secretion in perfused rat islets, requiring extracellular Ca2+ for the full expression of its effects. These effects may be exerted through a Ca2+-Ca2+ exchange over the cell membrane and/or through cAMP and intracellular Ca2+ perturbations.(ABSTRACT TRUNCATED AT 250 WORDS)

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