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Antiarrhythmic drugs, clofilium and cibenzoline are potent inhibitors of glibenclamide‐sensitive K + currents in Xenopus oocytes

Antiarrhythmic drugs, clofilium and cibenzoline are potent inhibitors of glibenclamide‐sensitive... 1 The novel K+ channel opener, Y‐26763 induced outward K+ currents in voltage‐clamped follicle‐enclosed Xenopus oocytes in a concentration‐dependent manner with an EC50 value of 58 μm. 2 The Y‐26763‐induced K+ current was completely and reversibly blocked by glibenclamide (an ATP‐sensitive K+ channel blocker) in a concentration‐dependent manner (IC50 140 nm). Effects of several antiarrhythmic drugs on Y‐26763‐induced glibenclamide‐sensitive K+ currents were investigated. 3 (±)‐Cibenzoline, RS‐2135, pirmenol, lorcainide and KW‐3407 (class I antiarrhythmic drugs, Na+ channel blockers) suppressed Y‐26763 responses in a concentration‐dependent manner with IC50 values (in μm) of 6.6, 54, 68, 71 and 370, respectively. 4 Clofilium, E‐4031, MS‐551 and bretylium (class III antiarrhythmic drugs which increase the action potential duration) also suppressed Y‐26763 responses concentration‐dependently, IC50 values (in μm) were 3.3, 660, 980 and ≥ 2000, respectively. N‐acetylprocainamide (class III antiarrhythmic drug) scarcely suppressed Y‐26763 responses. 5 The glibenclamide‐sensitive K+ currents elicted by KRN2391 were also suppressed by all these antiarrhythmic drugs. 6 The antiarrhythmic drugs, clofilium and (±)‐cibenzoline block glibenclamide‐sensitive K+ channels in Xenopus oocytes at concentrations comparable to their therapeutic plasma levels. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Pharmacology Wiley

Antiarrhythmic drugs, clofilium and cibenzoline are potent inhibitors of glibenclamide‐sensitive K + currents in Xenopus oocytes

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References (43)

Publisher
Wiley
Copyright
1993 British Pharmacological Society
ISSN
0007-1188
eISSN
1476-5381
DOI
10.1111/j.1476-5381.1993.tb13655.x
Publisher site
See Article on Publisher Site

Abstract

1 The novel K+ channel opener, Y‐26763 induced outward K+ currents in voltage‐clamped follicle‐enclosed Xenopus oocytes in a concentration‐dependent manner with an EC50 value of 58 μm. 2 The Y‐26763‐induced K+ current was completely and reversibly blocked by glibenclamide (an ATP‐sensitive K+ channel blocker) in a concentration‐dependent manner (IC50 140 nm). Effects of several antiarrhythmic drugs on Y‐26763‐induced glibenclamide‐sensitive K+ currents were investigated. 3 (±)‐Cibenzoline, RS‐2135, pirmenol, lorcainide and KW‐3407 (class I antiarrhythmic drugs, Na+ channel blockers) suppressed Y‐26763 responses in a concentration‐dependent manner with IC50 values (in μm) of 6.6, 54, 68, 71 and 370, respectively. 4 Clofilium, E‐4031, MS‐551 and bretylium (class III antiarrhythmic drugs which increase the action potential duration) also suppressed Y‐26763 responses concentration‐dependently, IC50 values (in μm) were 3.3, 660, 980 and ≥ 2000, respectively. N‐acetylprocainamide (class III antiarrhythmic drug) scarcely suppressed Y‐26763 responses. 5 The glibenclamide‐sensitive K+ currents elicted by KRN2391 were also suppressed by all these antiarrhythmic drugs. 6 The antiarrhythmic drugs, clofilium and (±)‐cibenzoline block glibenclamide‐sensitive K+ channels in Xenopus oocytes at concentrations comparable to their therapeutic plasma levels.

Journal

British Journal of Pharmacology – Wiley

Published: Jul 1, 1993

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