Referenced in: none

Automatically associated channels: Kv1.2 , Kv1.5 , Kv2.2 , Slo1

Title: Blocking of cloned and native delayed rectifier K channels from visceral smooth muscles by phencyclidine.

Authors: B W Frey, F T Lynch, J M Kinsella, B Horowitz, K M Sanders, A Carl

Journal, date & volume: Neurogastroenterol. Motil., 2000 Dec , 12, 509-16

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/11123705

Abstract
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 IdK(f)); (ii) a slowly activating, tetraethylammonium (TEA)-sensitive component (IdK(s)); and (iii) a rapidly activating, TEA-sensitive component, which has a steady-state inactivation curve shifted towards more negative potentials (IdK(n)). PCP blocked all three components with EC50 values of 45, 27 and 59 micromol 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 Ca2+-dependent outward current of large conductance Ca2+-activated K+ channels (BK channels).