Renal epithelial cells may have Mg
2+ transport pathways that regulate intracellular free Mg
2+ concentration ([Mg
2+]
i) and reabsorption into the body. In mag-fura 2 fluorescent measurement, extracellular Mg
2+ removal induced a Na
+-independent [Mg
2+]
i decrease. The [Mg
2+]
i decrease was suppressed by methyl arachidonyl fluorophosphonate, a cytosolic and Ca
2+-independent phospholipase A
2 (iPLA
2) inhibitor, and bromoenol lactone, an iPLA
2 inhibitor, but it was not suppressed by a secretory phospholipase A
2 inhibitor. On the contrary, the [Mg
2+]
i decrease was enhanced by the addition of exogenous arachidonic acid (AA). Next, we examined the effect of AA metabolite inhibitors on the [Mg
2+]
i decrease. 17-octadecynoic acid inhibited the [Mg
2+]
i decrease, but indomethacin and nordihydroguaiaretic acid did not. In the 17-octadecynoic acid-treated cells, 20-hydroxy-(5Z,8Z,11Z,14Z)-eicosatetraenoic acid (20-HETE) recovered the [Mg
2+]
i decrease. Nicardipine inhibited both the basal and the 20-HETE-enhanced [Mg
2+]
i decrease. These results suggest that 20-HETE is a key mediator in the activation of Na
+-independent Mg
2+ efflux.
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