Selective stimulation of glucagon secretion by β2‐adrenoceptors in isolated islets of Langerhans of the rat

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Abstract
1 In rat isolated islets of Langerhans the selective β2-adrenoceptor agonist, clenbuterol (1 to 20 μm), significantly increased the level of adenosine 3′:5′-cyclic monophosphate (cyclic AMP) within 2 min of incubation. 2 The cyclic AMP response to clenbuterol was inhibited in the presence of the selective β2 adrenoceptor antagonist, ICI 118551 (0.1 or 10 μm) but remained unchanged when the β1-antagonist, atenolol (0.1 μm) was administered. 3 Despite causing an elevation in cyclic AMP, clenbuterol (up to 20 μm) failed to influence insulin secretion at any glucose concentration tested, even in the presence of a phosphodiesterase inhibitor. 4 By contrast, clenbuterol elicited a dose-dependent rise in the rate of glucagon secretion; the maximal agonist-induced increase in secretion was two fold, a response equivalent to that observed with 20 mm l-arginine. 5 ICI 118551 significantly inhibited the rise in glucagon secretion induced by clenbuterol (up to 20 μm). 6 The results indicate that the rat islet A cell population is equipped with functional β2-adrenoceptors which influence glucagon secretion via the second messenger cyclic AMP, but that the B cells are deficient in functional β-receptors.