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Blockade by antiarrhythmic drugs of glibenclamide‐sensitive K + channels in Xenopus oocytes

Blockade by antiarrhythmic drugs of glibenclamide‐sensitive K + channels in Xenopus oocytes 1 The outward K+ current induced by KRN2391 (K+ channel opener) in Xenopus oocytes is blocked by glibenclamide. We have investigated the effects of various classes (I‐IV) of antiarrhythmic drugs on this KRN2391‐induced response. 2 All class I antiarrhythmic drugs (Na+ channel blockers) tested concentration‐dependently suppressed KRN2391‐induced responses with the rank order of potency (IC50 in μm), disopyramide (17.8) > aprindine (29.5) > propafenone (63.1) > ajmaline (145) > quinidine (151). Flecainide, SUN1165, lignocaine, mexiletine and procainamide were much less potent (IC50, 450– > 1000 μm) than quinidine. 3 The class II antiarrhythmic drugs (β‐blockers), timolol, (−)‐ and (±)‐ propranolol, and (+)‐propranolol (a non‐β‐blocker) inhibited KRN2391‐induced K+ currents in a concentration‐dependent manner with values for IC50 (μm) of 79, 131, 151 and 129, respectively, whilst butoxamine, oxprenolol, alprenolol, pindolol, nadolol, metoprolol and acebutolol were either weak (IC50, 300 μm — 600 μm) or virtually inactive (IC50, > 1000 μm). 4 The class III antiarrhythmic drugs, amiodarone and (+)‐sotalol scarcely affected KRN2391 responses. 5 All class IV drugs (Ca2+ antagonists) tested suppressed KRN2391‐induced responses in a concentration‐dependent manner with an IC50 of 6.3 μm for bepridil, 38 μm for prenylamine, 85 μm for verapamil and 135 μm for diltiazem. 6 In conclusion, antiarrhythmic drugs of classes I, II and IV potently blocked glibenclamide‐sensitive K+ channels in Xenopus oocytes. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Pharmacology Wiley

Blockade by antiarrhythmic drugs of glibenclamide‐sensitive K + channels in Xenopus oocytes

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References (42)

Publisher
Wiley
Copyright
1992 British Pharmacological Society
ISSN
0007-1188
eISSN
1476-5381
DOI
10.1111/j.1476-5381.1992.tb13407.x
Publisher site
See Article on Publisher Site

Abstract

1 The outward K+ current induced by KRN2391 (K+ channel opener) in Xenopus oocytes is blocked by glibenclamide. We have investigated the effects of various classes (I‐IV) of antiarrhythmic drugs on this KRN2391‐induced response. 2 All class I antiarrhythmic drugs (Na+ channel blockers) tested concentration‐dependently suppressed KRN2391‐induced responses with the rank order of potency (IC50 in μm), disopyramide (17.8) > aprindine (29.5) > propafenone (63.1) > ajmaline (145) > quinidine (151). Flecainide, SUN1165, lignocaine, mexiletine and procainamide were much less potent (IC50, 450– > 1000 μm) than quinidine. 3 The class II antiarrhythmic drugs (β‐blockers), timolol, (−)‐ and (±)‐ propranolol, and (+)‐propranolol (a non‐β‐blocker) inhibited KRN2391‐induced K+ currents in a concentration‐dependent manner with values for IC50 (μm) of 79, 131, 151 and 129, respectively, whilst butoxamine, oxprenolol, alprenolol, pindolol, nadolol, metoprolol and acebutolol were either weak (IC50, 300 μm — 600 μm) or virtually inactive (IC50, > 1000 μm). 4 The class III antiarrhythmic drugs, amiodarone and (+)‐sotalol scarcely affected KRN2391 responses. 5 All class IV drugs (Ca2+ antagonists) tested suppressed KRN2391‐induced responses in a concentration‐dependent manner with an IC50 of 6.3 μm for bepridil, 38 μm for prenylamine, 85 μm for verapamil and 135 μm for diltiazem. 6 In conclusion, antiarrhythmic drugs of classes I, II and IV potently blocked glibenclamide‐sensitive K+ channels in Xenopus oocytes.

Journal

British Journal of Pharmacology – Wiley

Published: Dec 1, 1992

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