The influence of sodium omission on alpha 2-adrenergic inhibition of insulin release by mouse islets.

The mechanisms by which activation of alpha 2-adrenoceptors inhibits insulin release are still incompletely understood. This study, performed with isolated mouse islets, identifies a possible role of Na+ in this inhibition. Regardless of the stimulus used to induce insulin release, the inhibitory effect of low concentrations of clonidine (0.01-0.1 microM) was markedly smaller in the absence of Na+ (with choline or lithium as substitute) than in its presence. The effectiveness of a high concentration of clonidine (1 microM) was, however, not affected by Na+ omission. The results indicate either that Na+ omission indirectly counteracts an effect of clonidine (e.g. on a membrane permeability or on Ca2+ handling), or that Na+ is directly involved in a cellular process (e.g. a Na+ current or the Na+/H+ exchange) controlled by alpha 2-adrenoceptors.