Elevation of cytosolic calcium by imidazolines in mouse islets of Langerhans: implications for stimulus‐response coupling of insulin release

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Abstract
1 Microfluorimetry techniques with fura-2 were used to characterize the effects of efaroxan (200 μm), phentolamine (200–500 μm) and idazoxan (200–500 μm) on the intracellular free Ca2+ concentration ([Ca2+]i) in mouse isolated islets of Langerhans. 2 The imidazoline receptor agonists efaroxan and phentolamine consistently elevated cytosolic Ca2+ by mechanisms that were dependent upon Ca2+ influx across the plasma membrane; there was no rise in [Ca2+]i when Ca2+ was removed from outside of the islets and diazoxide (100–250 μm) attenuated the responses. 3 Modulation of cytosolic [Ca2+]i by efaroxan and phentolamine was augmented by glucose (5–10 mM) which both potentiated the magnitude of the response and reduced the onset time of imidazoline-induced rises in [Ca2+]i. 4 Efaroxan- and phentolamine-evoked increases in [Ca2+]i were unaffected by overnight pretreatment of islets with the imidazolines. Idazoxan failed to increase [Ca2+]i under any experimental condition tested. 5 The putative endogenous ligand of imidazoline receptors, agmatine (1 μm-1 mM), blocked KATP channels in isolated patches of β-cell membrane, but effects upon [Ca2+]i could not be further investigated since agmatine disrupts fura-2 fluorescence. 6 In conclusion, the present study shows that imidazolines will evoke rises in [Ca2+]i in intact islets, and this provides an explanation to account for the previously described effects of imidazolines on KATP channels, the cell membrane potential and insulin secretion in pancreatic β-cells.

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