Modulation of potassium channels via the α1B-adrenergic receptor in human osteoblasts

Neurosci Lett. 2010 Nov 19;485(2):102-6. doi: 10.1016/j.neulet.2010.08.073. Epub 2010 Sep 15.

Abstract

Recent studies have demonstrated the involvement of the sympathetic nerve system in bone metabolism. We have previously demonstrated the expression of adrenergic receptors in the human osteoblast SaM-1 cell line. The aim of this study was to reveal the function of these receptors in osteoblasts using electrophysiological methods. During whole-cell patch clamp recording, the application of noradrenaline reduced the currents induced by a voltage ramp, and the effect was larger in the positive potential range. Pretreatment with the selective α(1B)-adrenergic receptor antagonist chloroethylclonidine eliminated the inhibitory effect of noradrenaline. Using Cs-based pipette solution to block potassium channels, the inhibitory effect of noradrenaline disappeared. In contrast, the effect was unaffected in the presence of tetraethylammonium (TEA), a potassium channel blocker. These results suggest that noradrenaline suppresses Cs-sensitive and TEA-insensitive potassium channels via the α(1B)-adrenergic receptor in human osteoblasts.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic alpha-Antagonists / pharmacology
  • Cell Line
  • Clonidine / analogs & derivatives
  • Clonidine / pharmacology
  • Humans
  • Male
  • Membrane Potentials / physiology*
  • Norepinephrine / metabolism
  • Norepinephrine / physiology
  • Osteoblasts / drug effects
  • Osteoblasts / metabolism*
  • Patch-Clamp Techniques / methods
  • Potassium Channel Blockers / pharmacology
  • Potassium Channels / metabolism*
  • Receptors, Adrenergic, alpha-1 / physiology*
  • Young Adult

Substances

  • Adrenergic alpha-Antagonists
  • Potassium Channel Blockers
  • Potassium Channels
  • Receptors, Adrenergic, alpha-1
  • chlorethylclonidine
  • Clonidine
  • Norepinephrine