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KMID : 0811720000040000015
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Korean Journal of Physiology & Pharmacology
2000 Volume.4 No. 0 p.15 ~ p.0
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Effects of Arachidonic Acid on the ATP-Sensitive K+ Currents in Murine Proximal Colonic Smooth Muscle Cells
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Jun Jae-Yeoul
Yeum Cheol-Ho
Yoon Pyung-Jin
Kong In-Deok
So In-Suk
Kim Ki-Whan
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Abstract
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ATP-sensitive K+ (KATP) channel has been shown to play an important role in the regulation of resting membrane potential. Arachidonic acid (AA) is a major component of cell membrane lipids released by either cellular damage or receptor-mediated stimulation of phospholipase A. AA and its metabolites generated by cyclooxygenase and lipoxygenase mediate various cell-signaling events. It has been reported that AA can modulate activities of several kinds of ionic currents. Therefore, to investigate modulatory effects of AA on the KATP channel of murine colonic smooth muscle cells, whole-cell patch clamp technique performed.
In current-calmp mode, AA induced membrane deploarization in normal bath solution. With 0.1 mM ATP and 140 mM K+ in the pipette and 90 mM K+ in the bath solution and a holding potential of -80 mV, pinacidil activated a glibenclamide-sensitive inward current. The reversal potential of these currents was reversed near to 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 in the pipette. Phorbol 12, 13-dibutyrate inhibited KATP currents, whereas 4-phorbol did not inhibited KATP currents. Chelerythrine did not inhibit the AA effects. Also, superoxide dismutase and metabolic inhibitors (indomethacine and NDGA) of AA did not affect on AA-induced inhibition. ETYA, nonmetabolizable AA analogue, inhibited KATP currents. These results suggest that AA may directly inhibit KATP currents. The inhibitory action is a possible mechanism of AA-induced membrane depolarization.
Source: Korean Journal of Physiology & Pharmacology.2000 Oct;4(Suppl):S12-S12
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