3-Morpholinosydnonimine as instigator of a glibenclamide-sensitive reduction in the insulin secretory rate.
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.
Antoine
M H
MH
Laboratory of Pharmacology, Université Libre de Bruxelles, School of Medicine, Brussels, Belgium.
Ouedraogo
R
R
Hermann
M
M
Segooris
J
J
Herchuelz
A
A
Lebrun
P
P
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
D015220:Calcium Channels; D007328:Insulin; D015221:Potassium Channels; C002385:linsidomine; D008981:Molsidomine; D005947:Glucose; D005905:Glyburide