Alpha₂-adrenoreceptor stimulation does not inhibit L-type calcium channels in mouse pancreatic β-cells

Abstract

The effects of α₂-adrenergic stimulation on the Ca²⁺-current in mouse pancreatic β-cells were investigated using the patch-clamp technique. When using the conventional whole-cell recording configuration (dialysis of cell interior with pipette solution), addition of adrenaline (1 μM) or the α₂-adrenergic agonist clonidine (5 μM) failed to reduce the Ca²⁺-current, irrespective of whether intracellular GTP (or GTPγ S) was present or not and at both physiological (1.3 mM) and elevated (10.2 mM) Ca²⁺-concentrations. In fact, in the absence of added guanine nucleotides, the agonists tended toincrease the Ca²⁺-current amplitude in the presence of the higher Ca²⁺-concentration. Ca²⁺-channel activation measured at 1.3 mM Ca²⁺ was not affected by clonidine. Half-maximal activation was observed at ≈−20 mV. In addition, when Ca²⁺-currents were recorded from intact β-cells, using the perforated patch whole-cell configuration, clonidine (1 μM) also failed to detectably affect the Ca²⁺-current. It is therefore suggested that the inhibition of β-cell electrical activity and insulin-secretion produced by α₂-adrenoreceptor stimulation does not result from suppression of the L-type Ca²⁺-current.