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- Title
Blocking of cloned and native delayed rectifier K<sup>+</sup> channels from visceral smooth muscles by phencyclidine.
- Authors
Frey, B. W.; Lynch, F. T.; Kinsella, J. M.; Horowitz, B.; Sanders, K. M.; Carl, A.
- 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 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 Ca2+-dependent outward current of large conductance Ca2+-activated K+ channels (BK channels).
- Subjects
PHENCYCLIDINE; POTASSIUM channels; SMOOTH muscle
- Publication
Neurogastroenterology & Motility, 2000, Vol 12, Issue 6, p509
- ISSN
1350-1925
- Publication type
Article
- DOI
10.1046/j.1365-2982.2000.00225.x