Abstract
In Madin-Darby canine kidney (MDCK) cells, the effect of 2-O-methyl PAF, an inactive analogue of platelet activating factor (PAF), on intracellular Ca 2+ concentration ([Ca 2+] i) was measured by using the Ca 2+-sensitive fluorescent dye fura-2. 2-O-methyl PAF (≥15 μM) caused a rapid rise of [Ca 2+] i in a concentration-dependent manner. 2-O-methyl PAF-induced [Ca 2+] i rise was partly reduced by removal of extracellular Ca 2+. 2-O-methyl PAF-induced extracellular Ca 2+ influx was also suggested by Mn 2+ influx-induced fura-2 fluorescence quench. The 2-O-methyl PAF-induced Ca 2+ influx was blocked by nifedipine, verapamil and diltiazem. In Ca 2+-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca 2+-ATPase, caused a monophasic [Ca 2+] i rise, after which 2-O-methyl PAF failed to increase [Ca 2+] i; also, pretreatment with 2-O-methyl PAF depleted thapsigargin-sensitive Ca 2+ stores. U73122, an inhibitor of phospholipase C, abolished ATP (but not 2-O-methyl PAF)-induced [Ca 2+] i rise. These findings suggest that 2-O-methyl PAF evokes a rapid increase in [Ca 2+] i in renal tubular cells by stimulating both extracellular Ca 2+ influx and intracellular Ca 2+ release.
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