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

Research output: Contribution to journalArticleResearchpeer-review

2 Citations (Scopus)

Abstract

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
Volume90
Issue number1
DOIs
StatePublished - 1 Sep 2002

Fingerprint

Arachidonic Acid
Smooth Muscle Myocytes
Adenosine Triphosphate
Glyburide
Baths
Protein Kinase C
Pinacidil
Acids
Protein C Inhibitor
Protein Kinase Inhibitors
GTP-Binding Proteins
Constriction
Indomethacin
Membrane Potentials
Superoxide Dismutase
Colon
Membranes

Keywords

  • ATP-sensitive K current
  • Arachidonic acid
  • Colonic smooth muscle

Cite this

Jun, J. Y., Yeum, C. H., Park, Y. W., Jang, I. Y., Kong, I. D., Sim, J. H., ... You, H. J. (2002). Effects of arachidonic acid on ATP-sensitive K+ current in murine colonic smooth muscle cells. Japanese Journal of Pharmacology, 90(1), 81-87. https://doi.org/10.1254/jjp.90.81
Jun, Jae Yeoul ; Yeum, Cheol Ho ; Park, Yoo Whan ; Jang, In Youb ; Kong, In Deok ; Sim, Jae Hoon ; So, Insuk ; Kim, Ki Whan ; You, Ho Jin. / Effects of arachidonic acid on ATP-sensitive K+ current in murine colonic smooth muscle cells. In: Japanese Journal of Pharmacology. 2002 ; Vol. 90, No. 1. pp. 81-87.
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abstract = "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.",
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Jun, JY, Yeum, CH, Park, YW, Jang, IY, Kong, ID, Sim, JH, So, I, Kim, KW & You, HJ 2002, 'Effects of arachidonic acid on ATP-sensitive K+ current in murine colonic smooth muscle cells', Japanese Journal of Pharmacology, vol. 90, no. 1, pp. 81-87. https://doi.org/10.1254/jjp.90.81

Effects of arachidonic acid on ATP-sensitive K+ current in murine colonic smooth muscle cells. / Jun, Jae Yeoul; Yeum, Cheol Ho; Park, Yoo Whan; Jang, In Youb; Kong, In Deok; Sim, Jae Hoon; So, Insuk; Kim, Ki Whan; You, Ho Jin.

In: Japanese Journal of Pharmacology, Vol. 90, No. 1, 01.09.2002, p. 81-87.

Research output: Contribution to journalArticleResearchpeer-review

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T1 - Effects of arachidonic acid on ATP-sensitive K+ current in murine colonic smooth muscle cells

AU - Jun, Jae Yeoul

AU - Yeum, Cheol Ho

AU - Park, Yoo Whan

AU - Jang, In Youb

AU - Kong, In Deok

AU - Sim, Jae Hoon

AU - So, Insuk

AU - Kim, Ki Whan

AU - You, Ho Jin

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N2 - 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.

AB - 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.

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