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

B W Frey1, F T Lynch, J M Kinsella

  • 1Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, USA.

Neurogastroenterology and Motility
|December 21, 2000
PubMed

Insights

Phencyclidine (PCP) blocks native and cloned delayed rectifier potassium (K+) currents in colonic myocytes. However, PCP does not affect large conductance calcium-activated potassium (BK) channels, indicating specific ion channel interactions.

Area of Science:

  • Pharmacology
  • Ion Channel Physiology
  • Gastrointestinal Physiology

Background:

  • Delayed rectifier potassium (K+) currents are crucial for regulating membrane potential in colonic smooth muscle.
  • Phencyclidine (PCP) is a dissociative anesthetic with known effects on neuronal ion channels.

Purpose of the Study:

  • To investigate the impact of phencyclidine (PCP) on native and cloned delayed rectifier K+ currents in colonic myocytes.
  • To determine if PCP affects other types of potassium channels, such as large conductance calcium-activated potassium (BK) channels.

Main Methods:

  • Voltage-clamp techniques were employed to study native K+ currents in canine circular colonic myocytes.
  • Cloned K+ channels (Kv1.2, Kv1.5, Kv2.2) were expressed in Xenopus oocytes for functional analysis.
  • The effects of PCP on different K+ current components and BK channels were quantified.

Main Results:

  • PCP effectively blocked three distinct components of native delayed rectifier K+ currents (IdK(f), IdK(s), IdK(n)) with varying potencies.
  • PCP demonstrated similar blocking potency against cloned canine (Kv1.2, Kv1.5) and human (Kv2.2) delayed rectifier K+ channels.
  • PCP did not inhibit the Ca2+-dependent outward current mediated by large conductance calcium-activated potassium (BK) channels.

Conclusions:

  • Phencyclidine (PCP) is a potent blocker of delayed rectifier potassium channels in colonic smooth muscle.
  • The findings suggest that PCP's effects on colonic function may involve specific interactions with Kv channel subtypes.
  • PCP does not appear to modulate BK channels, indicating a selective ion channel pharmacology in this tissue.

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