Blocking of cloned and native delayed rectifier K+ channels from visceral smooth muscles by phencyclidine

We investigated the effect of phencyclidine (PCP) on three native delayed r ectifier K+ currents and three channels cloned from canine and human circul ar colonic myocytes using voltage-clamp techniques. Native delayed rectifie r K+ current in canine circular colon is composed of at least three compone nts: (i) a rapidly activating, 4-aminopyridine-sensitive component (termed I-dK(f)); (ii) a slowly activating, tetraethylammonium (TEA)-sensitive comp onent (I-dK(s)); and (iii) a rapidly activating, TEA-sensitive component, w hich has a steady-state inactivation curve shifted towards more negative po tentials (I-dK(n)). PCP blocked all three components with EC50 values of 45 , 27 and 59 mu mol L-1, respectively. Blocking was neither use-dependent no r voltage-dependent. Delayed rectifier K+ channels cloned from canine (Kv1. 2, Kv1.5) and from human (Kv2.2) colon were expressed in Xenopus oocytes. P CP 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 cur rent of large conductance Ca2+-activated K+ channels (BK channels).