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  • Title: Selective alpha 2-adrenoceptor activation by clonidine: effects on 45Ca2+ efflux and insulin secretion from isolated rat islets.
    Author: Skoglund G, Lundquist I, Ahrén B.
    Journal: Acta Physiol Scand; 1988 Mar; 132(3):289-96. PubMed ID: 2465665.
    Abstract:
    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.
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