Effects of Extracellular ATP on Ca 2+ Mobilization in Madin Darby Canine Kidney (MDCK) Cells

Pei Shan Liu*, Mei Ying Ho, Hsi Lung Hsieh


研究成果: 期刊稿件文章同行評審

2 引文 斯高帕斯(Scopus)


Previous studies have demonstrated that ATP activates calcium-dependent K + channels thereby leading to plasma membrane hyperpolarization and chloride secretion in MDCK cells. However, the signaling pathway involved in regulating ATP-evoked Ca 2+ mobilization in MDCK cells remains unclarified. The present study was performed to elucidate the mechanisms underlying ATP-evoked calcium mobilization and inositol phospholipid turnover in MDCK cells. Our results indicate that ATP exerted its effects by activating the P 2u subtype purinoceptor because both ATP and UTP but not adenosine caused Ca 2+ mobilization. ATP induced (Ca 2+ ] i increase in a dose-dependent manner with a maximal and half-maximal effect at 100 μM and 5 μM, respectively. In the absence of external Ca 2+ , both UTP and ATP were capable of mobilizing Ca 2+ from internal stores through an IPS-sensitive pathway and the response for the former was larger than the latter. While in the presence of external Ca 2+ , the magnitude of UTP-induced [Ca 2+ ] i increase was similar to that of ATP. These observations suggest that other mechanisms involved in addition to P 2u subtype receptors in regulating ATP-induced Ca 2+ response. The Ca 2+ transients observed in Mg 2+ -depleted media were greater than those seen in Mg 2+ -contained media. ATP-induced Na + influx were evidenced by SBFI loaded MDCK cells in Mg 2+ -depleted media. These data support that non-selective ATP 4 membrane pores were formed under the application of ATP. The ATP-induced Ca 2+ rise was suppressed by either ω-conotoxin or La 3+ but was unaffected by the L-type Ca 2+ channel blockers, verapamil and nifedipine. The deprivation of external Na + also enhanced the ATP-induced Ca 2+ rise. These data indicate that a P 2 receptor-mediated cation channel was also involved under the stimulation of ATP.

頁(從 - 到)189-196
期刊Chinese Journal of Physiology
出版狀態已出版 - 1996


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