Activation of alpha adrenergic and muscarinic receptors modifies early glucose suppression of cytoplasmic Ca2+ in pancreatic beta-cells
2014 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 445, no 3, 629-632 p.Article in journal (Refereed) Published
Elevation of glucose induces transient inhibition of insulin release by lowering cytoplasmic Ca2+([Ca2+](i)) below baseline in pancreatic beta-cells. The period of [Ca2+], decrease (phase 0) coincides with increased glucagon release and is therefore the starting point for antisynchronous pulses of insulin and glucagon. We now examine if activation of adrenergic alpha(2A) and muscarinic M-3 receptors affects the initial [Ca2+](i) response to increase of glucose from 3 to 20 mM in beta-cells situated in mouse islets. In the absence of receptor stimulation the elevation of glucose lowered [Ca2+](i) during 90-120 s followed by rise due to opening of voltage-dependent Ca2+ channels. The period of [Ca2+](i) decrease was prolonged by activation of the alpha 2A adrenergic receptors (1 mu M epinephrine or 100 nM clonidine) and shortened by stimulation of the muscarinic M-3 receptors (0.1 mu.M acetylcholine). The latter effect was mimicked by the Na/K pump inhibitor ouabain (10-100 mu M). The results indicate that prolonged initial decrease (phase 0) is followed by slow [Ca2+](i) rise and shorter decrease followed by fast rise. It is concluded that the period of initial decrease of [Ca2+](i); regulates the subsequent beta-cell response to glucose.(C) 2014 Elsevier Inc. All rights reserved.
Place, publisher, year, edition, pages
2014. Vol. 445, no 3, 629-632 p.
Acetylcholine, beta-cell, Cytoplasmic Ca2+, Epinephrine, Glucose, Ouabain
Cell and Molecular Biology
IdentifiersURN: urn:nbn:se:uu:diva-225102DOI: 10.1016/j.bbrc.2014.02.056ISI: 000334323100016OAI: oai:DiVA.org:uu-225102DiVA: diva2:719899