Stimulation of insulin secretion by efaroxan may involve interaction with potassium channels.

The imidazoline alpha 2-antagonist efaroxan was found to stimulate insulin secretion from isolated rat pancreatic islets incubated in glucose concentrations between 4 and 12 mM. This response could not be attributed to interaction of efaroxan with either classical alpha 2-receptors or with a B-cell 'imidazoline receptor', since the effect was not reproduced by the structural analogue idazoxan. Stimulation of insulin secretion by efaroxan correlated with the ability of the drug to reverse the inhibition of secretion mediated by the potassium channel agonist diazoxide. The data suggest that the capacity of efaroxan to stimulate insulin secretion may be related to an interaction with potassium channels in the pancreatic B-cell.