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Selective alpha 2-adrenoceptor activation by clonidine: effects on 45Ca2+ efflux and insulin secretion from isolated rat islets

, : Selective alpha 2-adrenoceptor activation by clonidine: effects on 45Ca2+ efflux and insulin secretion from isolated rat islets. Acta Physiologica Scandinavica 132(3): 289-296

A possible role for Ca2+ in the alpha-adrenoceptor-induced inhibition of glucose-stimulated insulin secretion was studied in isolated rat islets by the use of the selective alpha 2-adrenoceptor agonist clonidine. We found that clonidine, in contrast to the alpha 1-adrenoceptor agonist phenylephrine, inhibited glucose-stimulated insulin secretion at dose levels below 10(-6) mol l-1. In islets preloaded with 45Ca2+ and perifused at 2 mmol l-1 Ca2+, clonidine (10(-6) mol l-1) reduced the glucose (13.3 mmol l-1)-stimulated 45Ca2+ 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 alpha 2-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.


PMID: 2465665

DOI: 10.1111/j.1748-1716.1988.tb08332.x

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