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4‐aminopyridine activates potassium currents by activation of a muscarinic receptor in feline atrial myocytes.
Author(s) -
Navarro-Polanco R A,
Sánchez-Chapula J A
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1997.sp021891
Subject(s) - muscarinic acetylcholine receptor , 4 aminopyridine , potassium channel , chemistry , patch clamp , biophysics , inward rectifier potassium ion channel , acetylcholine , membrane potential , medicine , myocyte , potassium channel blocker , cardiac transient outward potassium current , endocrinology , voltage clamp , pertussis toxin , pacemaker potential , atropine , ion channel , receptor , g protein , biochemistry , biology
1. The effects of 4‐aminopyridine (4‐AP) on action potentials, macroscopic membrane currents and single‐channel recording from cardiac left atrial myocytes of the adult cat were studied using the whole‐cell and cell‐attached configurations of the patch‐clamp technique. 2. 4‐AP (1 mM) produced a hyperpolarization of the resting membrane potential and a shortening of action potential duration. Under voltage‐clamp conditions, we have found that 4‐AP increased a background current and a delayed rectifier outward current. These effects were antagonized by atropine. In addition, both effects seemed to be mediated through a pertussis toxin‐sensitive G protein. 3. The background current induced by 4‐AP displayed properties that are highly similar to those of the inwardly rectifying potassium current activated by acetylcholine (IK(ACh)). The time‐dependent potassium current activated by 4‐AP has kinetic and pharmacological properties different from those of the delayed rectifier potassium current previously identified in cardiac myocytes. 4. The activation of the delayed rectifier‐like potassium current could be explained by the activation of a novel muscarinic receptor subtype in which acetylcholine acts as the antagonist. Another possibility is that 4‐AP activates IK(ACh) in a time‐ and voltage‐dependent manner.