Effects of Arachidonic Acid on ATP-Sensitive K+ Current in Murine Colonic Smooth Muscle Cells

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 a...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 2002, Vol.90(1), pp.81-87
Main Authors: Jun, Jae Yeoul, Yeum, Cheol Ho, Park, Yoo Whan, Jang, In Youb, Kong, In Deok, Sim, Jae Hoon, So, Insuk, Kim, Ki Whan
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - physiology
Animals
Arachidonic acid
Arachidonic Acid - pharmacology
ATP-sensitive K+ current
Colon - drug effects
Colon - physiology
Colonic smooth muscle
Female
Male
Membrane Potentials - drug effects
Membrane Potentials - physiology
Mice
Mice, Inbred BALB C
Myocytes, Smooth Muscle - drug effects
Myocytes, Smooth Muscle - physiology
Potassium Channels - physiology
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Summary: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.
ISSN:0021-5198
1347-3506
DOI:10.1254/jjp.90.81