Mechanisms of Rise and Decay of ADP-Evoked Calcium Signal in MDCK Cells

Chung Ren Jan, Chin Man Ho, Sheng Nan Wu, Ching Jiunn Tseng

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


We have studied the effects of ADP on intracellular calcium levels ([Ca 2+ ]j) measured by fura-2 fluorimetry in Madin Darby canine kidney (MDCK) cells. ADP evoked [Ca 2+ ] i rises dose-dependently by releasing Ca 2+ from the inositol 1,4,5-trisphosphate (IP 3 )-dependent Ca 2+ pool followed by capacitative Ca 2+ entry. The Ca 2+ signal consisted of a peak and a gradual decline which reached a plateau in the case of 0.1-1 mM ADP; a plateau was not seen in the response to 10 mM ADP. ADP acted by stimulating P 2u and P 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 2+ pumps might play important roles in the decay of the Ca 2+ signal. The Ca 2+ signal was dramatically inhibited by 100 μM LaCl 3 .

Original languageEnglish
Pages (from-to)67-73
Number of pages7
JournalChinese Journal of Physiology
Issue number2
Publication statusPublished - 1998 Jun 30

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)


Dive into the research topics of 'Mechanisms of Rise and Decay of ADP-Evoked Calcium Signal in MDCK Cells'. Together they form a unique fingerprint.

Cite this