[Status of ATP-dependent K+-channels of pancreatic beta-cells exposed to a series of sulfonylurea drugs].
The authors analyze the relationships between electrophysiologic processes taking place on beta-cell membranes under the effects of some second generation sulfonylurea drugs: gliclazide, glibenclamide, and glipizide and their secretogenic effects on insulin secretion. All the tested drugs induced complete blocking of K(+)-ATP-dependent channels when administered in concentrations from 1 to 20 microM (physiologic doses). Glucose had a similar effect. The canal is closed very soon, within 30 sec, and is closed for approximately 10 min, rapidly opening after the drug is washed away. Reduced activity of the channels up to their closure is conducive to the onset of insulin secretion. Glibenclamide proved to be the most potent suppressor of individual channel activity, this being confirmed by its more potent hypoglycemic effect as compared to gliclazide or glipizide.
Babichev
V N
VN
Ignat'ev
N S
NS
Balabolkin
M I
MI
D000255:Adenosine Triphosphate / Q000502:physiology*; D005907:Gliclazide / Q000494:pharmacology*; D005913:Glipizide / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D015221:Potassium Channels / Q000187:drug effects*
D007328:Insulin; D015221:Potassium Channels; D000255:Adenosine Triphosphate; D005907:Gliclazide; D005947:Glucose; D005905:Glyburide; D005913:Glipizide
Sostoianie ATF-zavisimykh K+-kanalov beta-kletok podzheludochnoĭ zhelezy pod vliianiem riada sul'fonilmochevinnykh preparatov.