Selective α2‐adrenoceptor activation by clonidine: effects on45Ca2efflux and insulin secretion from isolated rat islets

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Abstract
A possible role for Ca2+in the α‐adrenoceptor‐induced inhibition of glucose‐stimulated insulin secretion was studied in isolated rat islets by the use of the selective α2‐adrenoceptor agonist clonidine. We found that clonidine, in contrast to the a,‐adrenoceptor agonist phenylephrine, inhibited glucose‐stimulated insulin secretion at dose levels below 10‐6mol l‐1. In islets preloaded with46Ca2+and perifused at 2 mmol llCa2+, clonidine (10‐6moll‐1) reduced the glucose (13.3 mmol l‐1)‐stimulated46Ca2+efflux during both the first and second phases of insulin secretion. Furthermore, the inhibitory effect of clonidine on glucose (13.3 mmol l‐1)‐stimulated insulin secretion was partially counteracted by raising the extracellular Ca2+concentrations. Moreover, the calcium channel agonist Bay K 8644 counteracted the inhibition by clonidine on glucose‐stimulated insulin secretion. Our results suggest that selective α2‐adrenoceptor‐induced inhibition of glucose‐stimulated insulin secretion is mediated, at least partially, by restraint of Ca2+‐influx. This action might in turn be exerted through interference with the voltage‐dependent calcium channels.