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Action of nicorandil on ATP‐sensitive K + channel in guinea‐pig ventricular myocytes
Author(s) -
Nakayama Keiko,
Fan Zheng,
Marumo Fumiaki,
Sawanobori Tohru,
Hiraoka Masayasu
Publication year - 1991
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1991.tb09841.x
Subject(s) - nicorandil , glibenclamide , pinacidil , chemistry , biophysics , patch clamp , medicine , myocyte , adenosine triphosphate , inward rectifier potassium ion channel , intracellular , electrophysiology , endocrinology , biochemistry , ion channel , biology , receptor , diabetes mellitus
1 Patch‐clamp techniques were used to study the effects of nicorandil (2‐nicotinamiodethyl nitrate) on the adenosine 5′‐triphosphate (ATP)‐sensitive K + channel current ( I K.ATP ) in guinea‐pig ventricular myocytes. 2 Nicorandil activated the time‐independent outward current. This effect was dependent on intracellular ATP concentration ([ATP] i ) showing a larger effect at 2 m m than at 10 m m [ATP] i The nicorandil‐induced outward current was inhibited by application of 0.3 μ m glibenclamide. 3 In the inside‐out patch configuration, 0.3–1.0 m m nicorandil increased the open‐state probability of I K.ATP without a change in its conductance value (about 90pS). This effect was inhibited by glibenclamide. Analysis of the open and closed time distributions showed that nicorandil had no effect on open and closed distributions shorter than 5 ms. On the other hand, nicorandil increased the life time of bursts and decreased the interburst intervals. 4 The inward rectifier K + channel current was not influenced by internal application of nicorandil. 5 Therefore, we conclude that I K.ATP is the only K + current activated by nicorandil, and the main effect of nicorandil is on the kinetics of the I K.ATP bursting behaviour. These actions are similar to that of pinacidil on this preparation.