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The oral hypoglycemie agent, U‐56324, inhibits the activity of ATP‐sensitive potassium channels in cell‐free membrane patches from cultured mouse pancreatic B‐cells
Author(s) -
Hopkins William F.,
Fatherazi Sahba,
Cook Daniel L.
Publication year - 1990
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(90)80818-4
Subject(s) - potassium channel , potassium , chemistry , biophysics , calcium activated potassium channel , biochemistry , membrane potential , inward rectifier potassium ion channel , biology , ion channel , receptor , organic chemistry
U‐56324, a hypoglycemic agent derived from nicotinic acid, inhibited the activity of ATP‐sensitive potassium channels in excised patches from mouse pancreatic B‐cells. The effect of U‐56324 on channel activity was reversible and concentration‐dependent while it had no effect on single channel conductance. The positional isomer, U‐59588, which has relatively little hypoglycemic activity, had no effect on channel properties. U‐56324, at the same concentrations, had no effect on calcium‐activated potassium channels. The basis for the potentially antidiabetic properties of U‐56324 may therefore be due to direct and specific inhibition of ATP‐sensitive potassium channels.