title: The influence of sodium omission on alpha 2-adrenergic inhibition of insulin release by mouse islets.
abstract: 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.
authors.affiliation: Unité de Diabétologie et Nutrition, University of Louvain, Faculty of Medicine, Brussels, Belgium.
authors.forename: G
authors.initials: G
authors.lastname: Bertrand
authors.forename: J C
authors.initials: JC
authors.lastname: Henquin
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002794:Choline / Q000494:pharmacology; D003000:Clonidine / Q000494:pharmacology*; D005110:Extracellular Space / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D051379:Mice; D008815:Mice, Inbred Strains; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D000317:Adrenergic alpha-Antagonists; D007328:Insulin; D003994:Bucladesine; D012964:Sodium; D005947:Glucose; D003000:Clonidine; D002794:Choline; D011188:Potassium