Abstract.
Several α2-adrenoceptor agonists containing an imidazoline moiety inhibit insulin secretion when applied to beta cells. In the present study we investigated such imidazolines in regard to membrane potential effects in MIN 6 cells. We confirmed the inhibition of insulin release as reported in previous studies and showed an additional hyperpolarizing activity of the imidazolines using bisoxonol for membrane potential measurements. Pertussis toxin pre-incubation of MIN 6 cells converted the inhibitory imidazoline activity with regard to insulin release into a stimulatory effect. In addition, the marked hyperpolarization caused by the α-adrenoceptor agonists containing an imidazoline moiety was converted into a depolarizing effect after pertussis toxin pre-incubation. Adrenaline, an α-adrenoceptor agonist lacking an imidazoline moiety, also inhibited insulin release and hyperpolarized MIN 6 cells. Pertussis toxin pre-incubation led only to a loss of the inhibitory adrenaline effect and of the hyperpolarization but not to the stimulatory effects observed with the imidazolines. Thus a stimulatory effect of α-adrenoceptor agonists containing an imidazoline moiety was demasked by PTX in this study. It remains to be clarified to which extent a blockade of KATP channels is responsible for this effect.
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Scheltdorf, M., Mest, HJ. Pertussis toxin converts hyperpolarizations caused by α2-adrenoceptor agonists containing an imidazoline moiety into depolarizations in MIN 6 cells. Naunyn-Schmiedeberg's Arch Pharmacol 366, 204–208 (2002). https://doi.org/10.1007/s00210-002-0612-4
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DOI: https://doi.org/10.1007/s00210-002-0612-4