Effects of arachidonic acid on ATP-sensitive K+ current in murine colonic smooth muscle cells

Jae Yeoul Jun, Cheol Ho Yeum, Yoo Whan Park, In Youb Jang, In Deok Kong, Jae Hoon Sim, Insuk So, Ki Whan Kim, Ho Jin You

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1 Citation (Scopus)


The effects of arachidonic acid (AA) and the mechanism through which it modulates ATP-sensitive K+ (KATP) currents were examined in single smooth muscle cells of murine proximal colon. In the current-clamping mode, AA and glibenclamide induced depolarization of membrane potential. Using 0.1 mM ATP and 140 mM K+ solution in the pipette and 90 mM K+ in the bath solution at a -80 mV of holding potential, pinacidil activated the glibenclamide-sensitive inward current. The potential of these currents was reversed to near the equilibrium potential of K+ by 60 mM K+ in the bath solution. AA inhibited KATP currents in a dose-dependent manner. This inhibition was not changed when 1 mM GDPβS was present in the pipette. Chelerythrine, protein kinase C inhibitor, did not block the AA effects. Superoxide dismutase and metabolic inhibitors (indomethacin and nordihydroguaiacretic acid) of AA did not affect the AA-induced inhibition. Eicosatetraynoic acid, a nonmetabolizable analogue of AA, inhibited the KATP currents. These results suggest that AA-induced inhibition of KATP currents is not mediated by G-protein or protein kinase C activation. The inhibitory action is likely to be a possible mechanism of AA-induced membrane depolarization.

Original languageEnglish
Pages (from-to)81-87
Number of pages7
JournalJapanese Journal of Pharmacology
Issue number1
Publication statusPublished - 2002 Sept 1

All Science Journal Classification (ASJC) codes

  • Pharmacology


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