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Blocking of cloned and native delayed rectifier K + channels from visceral smooth muscles by phencyclidine
Author(s) -
Frey B. W.,
Lynch F. T.,
Kinsella J. M.,
Horowitz B.,
Sanders K. M.,
Carl A.
Publication year - 2000
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1046/j.1365-2982.2000.00225.x
Subject(s) - tetraethylammonium , chemistry , biophysics , patch clamp , xenopus , repolarization , charybdotoxin , potassium channel , inward rectifier potassium ion channel , electrophysiology , ion channel , membrane potential , biochemistry , medicine , biology , potassium , receptor , organic chemistry , gene
We investigated the effect of phencyclidine (PCP) on three native delayed rectifier K + currents and three channels cloned from canine and human circular colonic myocytes using voltage‐clamp techniques. Native delayed rectifier K + current in canine circular colon is composed of at least three components: (i) a rapidly activating, 4‐aminopyridine‐sensitive component (termed I dK(f) ); (ii) a slowly activating, tetraethylammonium (TEA)‐sensitive component (I dK(s) ); and (iii) a rapidly activating, TEA‐sensitive component, which has a steady‐state inactivation curve shifted towards more negative potentials (I dK( n ) ). PCP blocked all three components with EC 50 values of 45, 27 and 59 μmol L –1 , respectively. Blocking was neither use‐dependent nor voltage‐dependent. Delayed rectifier K + channels cloned from canine (Kv1.2, Kv1.5) and from human (Kv2.2) colon were expressed in Xenopus oocytes. PCP blocked all three currents with similar potency. In contrast, PCP (up to 10 –4 mol L –1 ) did not reduce the magnitude of Ca 2+ ‐dependent outward current of large conductance Ca 2+ ‐activated K + channels (BK channels).