Swelling-activated and arachidonic acid-induced currents are TREK-1 in rat bladder smooth muscle cells

Fukushima J Med Sci. 2016 Jun 8;62(1):18-26. doi: 10.5387/fms.2015-20. Epub 2016 Feb 25.


Using the perforated patch voltage clamp, we investigated swelling-activated ionic channels (SACs) in rat urinary bladder smooth muscle cells. Hypo-osmotic (60%) bath solution increased a membrane current which was inhibited by the SAC inhibitor, gadolinium. The reversal potential of the hypotonicity-induced current shifted in the positive direction by increasing external K(+) concentration. The hypotonicity-induced current was inhibited by extracellular acidic pH, phorbol ester and forskolin. These pharmacological properties are identical to those of arachidonic acid-induced current present in these cells, suggesting the presence of TREK-1, a four-transmembrane two pore domain K(+) channel. Using RT-PCR we screened rat bladder smooth muscles and cerebellum for expression of TREK-1, TREK-2 and TRAAK mRNAs. Only TREK-1 mRNA was expressed in the bladder, while all three were expressed in the cerebellum. We conclude that a mechanosensitive K(+) channel is present in rat bladder myocytes, which is activated by arachidonic acid and most likely is TREK-1. This K(+) channel may have an important role in the regulation of bladder smooth muscle tone during urine storage.

MeSH terms

  • Animals
  • Arachidonic Acid / pharmacology*
  • Colforsin / pharmacology
  • Hydrogen-Ion Concentration
  • Male
  • Membrane Potentials / drug effects
  • Muscle, Smooth / physiology*
  • Potassium Channels, Tandem Pore Domain / physiology*
  • Rats
  • Rats, Sprague-Dawley
  • Tetradecanoylphorbol Acetate / pharmacology
  • Urinary Bladder / physiology*


  • Potassium Channels, Tandem Pore Domain
  • potassium channel protein TREK-1
  • Colforsin
  • Arachidonic Acid
  • Tetradecanoylphorbol Acetate