Alpha 2-adrenergic stimulation counteracts glucose-induced rise of sodium in pancreatic islets exposed to ouabain.

The effects of alpha 2-adrenergic activation by clonidine on sodium handling were analysed in beta-cell-rich pancreatic mouse islets. In the steady-state situation, clonidine (1 microM) amplified lowering of sodium induced by 20 mM glucose, while the content remained unchanged in 3mM glucose. The loss of sodium in Na(+)-deficient medium was stimulated by glucose but was not affected by clonidine. This agonist also did not influence the ouabain-induced uptake of sodium at 3 mM glucose but partially counteracted additional uptake in response to 20 mM glucose. Although lacking effects of its own, 5 microM yohimbine completely counteracted the action of clonidine. The glucose amplification of the ouabain-induced uptake of sodium was suppressed also by 10 microM of the Ca(2+)-channel blockers methoxyverapamil and diltiazem. Both tolbutamide (100 microM) and dibutyryl cyclic AMP (1 mM) mimicked the action of glucose by promoting clonidine-sensitive uptake of sodium in the presence of ouabain. It is concluded that activation of alpha 2-adrenoceptors has profound effects on the sodium handling of pancreatic beta-cells exposed to glucose and other stimulators of insulin release.