Premium
Quinine inhibits Ca 2+ ‐independent K + channels whereas tetraethylammonium inhibits Ca 2+ ‐activated K + channels in insulin‐secreting cells
Author(s) -
Findlay Ian,
Dunne Mark J.,
Ullrich Susanne,
Wollheim Claes B.,
Petersen Ole H.
Publication year - 1985
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(85)80729-8
Subject(s) - tetraethylammonium , conductance , channel blocker , chemistry , membrane potential , inward rectifier potassium ion channel , biophysics , potassium channel , patch clamp , analytical chemistry (journal) , ion channel , biochemistry , potassium , chromatography , biology , physics , calcium , receptor , organic chemistry , condensed matter physics
The effects of quinine and tetraethylammonium (TEA) on single‐channel K + currents recorded from excised membrane patches of the insulin‐secreting cell line RINm5F were investigated. When 100 μM quinine was applied to the external membrane surface K + current flow through inward rectifier channels was abolished, while a separate voltage‐activated high‐conductance K + channel was not significantly affected. On the other hand, 2 mM TEA abolished current flow through voltage‐activated high‐conductance K + channels without influencing the inward rectifier K + channel. Quinine is therefore not a specific inhibitor of Ca 2+ ‐activated K + channels, but instead a good blocker of the Ca 2+ ‐independent K + inward rectifier channel whereas TEA specifically inhibits the high‐conductance voltage‐activated K + channel which is also Ca 2+ ‐activated.