title: 3-Morpholinosydnonimine as instigator of a glibenclamide-sensitive reduction in the insulin secretory rate.
abstract: The nitric oxide (NO) donor SIN-1 (3-morpholinosydnonimine) induced a concentration-dependent inhibition of the secretory response to glucose. The negative insulinotropic action of SIN-1 was attenuated by the hypoglycemic sulfonylurea glibenclamide. Moreover, the NO donor enhanced 86Rb outflow from perfused islets and reduced the glucose-induced increase in 45Ca outflow. The present data provide further evidence that NO donors impair the secretory response to glucose, at least in part, by activating the ATP-sensitive K+ channels.
authors.affiliation: Laboratory of Pharmacology, Université Libre de Bruxelles, School of Medicine, Brussels, Belgium.
authors.forename: M H
authors.initials: MH
authors.lastname: Antoine
authors.forename: R
authors.initials: R
authors.lastname: Ouedraogo
authors.forename: M
authors.initials: M
authors.lastname: Hermann
authors.forename: J
authors.initials: J
authors.lastname: Segooris
authors.forename: A
authors.initials: A
authors.lastname: Herchuelz
authors.forename: P
authors.initials: P
authors.lastname: Lebrun
mesh_terms: D000818:Animals; D015220:Calcium Channels / Q000187:drug effects; D015536:Down-Regulation; D004347:Drug Interactions; D005947:Glucose; D005905:Glyburide / Q000494:pharmacology*; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects*; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D012636:Secretory Rate / Q000187:drug effects
chemical_list: D015220:Calcium Channels; D007328:Insulin; D015221:Potassium Channels; C002385:linsidomine; D008981:Molsidomine; D005947:Glucose; D005905:Glyburide