ALPHA-2-ADRENOCEPTOR STIMULATION DOES NOT INHIBIT L-TYPE CALCIUM CHANNELS IN MOUSE PANCREATIC BETA-CELLS

The effects of alpha-2-adrenergic stimulation on the Ca2+-current in mouse pancreatic beta-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-mu-M) or the alpha-2-adrenergic agonist clonidine (5-mu-M) failed to reduce the Ca2+-current, irrespective of whether intracellular GTP (or GTP-gamma 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 to increase 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 almost-equal-to -20 mV. In addition, when Ca2+-currents were recorded from intact beta-cells, using the perforated patch whole-cell configuration, clonidine (1-mu-M) also failed to detectably affect the Ca2+-current. It is therefore suggested that the inhibition of beta-cell electrical activity and insulin-secretion produced by alpha-2-adrenoreceptor stimulation does not result from suppression of the L-type Ca2+-current.