- 期刊
Mechanisms of Rise and Decay of ADP-Evoked Calcium Signal in MDCK Cells
並列摘要
We have studied the effects of ADP on intracellular calcium levels ([Ca(superscript 2+)](subscript i) measured by fura-2 fluorimetry in Madin Darby canine kidney (MDCK) cells. ADP evoked [Ca(superscript 2+)](subscript i) rises dose-dependently by releasing Ca(superscript 2+) from the inositol 1,4,5-trisphosphate (IP3)-dependent Ca(superscript 2+) pool followed by capacitative Ca(superscript 2+) entry. The Ca(superscript 2+) signal consisted of a peak and a gradual decline which reached a plateau in the case of 0.1-1mM ADP; a plateau was not seen in the response to 10mM ADP. ADP acted by stimulating P(subscript 2u) and P(subscript 2y), receptors based on rank order of agonist potency: ATP=UTP＞ADP＞2-methylthio-ATP＞2-methylthio-ADP＞adenosine＞α, β-methylene ATP. Buffering by lysosomes and efflux via plasmalemmal Ca(superscript 2+) pumps might play important roles in the decay of the Ca(superscript 2+) signal. The Ca(superscript 2+) signal was dramatically inhibited by 100μM LaCl3.
延伸閱讀
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