Effect of capsazepine on [Ca2+]i in MDCK renal tubular cells

Jeng Yu Tsai, Chun Chi Kuo, Chiang Ting Chou, David Chao, He Hsiung Cheng, Jue Long Wang, Jin Shiung Cheng, Ko Long Lin, Jong Khing Huang, Hong Tai Chang, Chung Ren Jan*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review


The current study explored whether capsazepine changed basal cytosolic free Ca2+ concentrations ([Ca2+]i) levels in suspended Madin Darby canine kidney (MDCK) cells cells by using fura-2 as a Ca2+-selective fluorescent dye. At concentrations of 10-200 μM, capsazepine increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was partially reduced by 40% by removing extracellular Ca2+. Capsazepine induced Mn2+ quench of fura-2 fluorescence, indirectly implicating Ca2+ entry. Capsazepine-induced Ca2+ influx was unchanged by L-type Ca 2+ entry inhibitors and protein kinase C modulators [phorbol 12-myristate 13-acetate (PMA) and GF109203X]. In Ca2+-free medium, 100 μM capsazepine-induced Ca2+ release was substantially suppressed by pretreatment with thapsigargin (an endoplasmic reticulum Ca 2+ pump inhibitor). Pretreatment with capsazepine nearly abolished thapsigargin-induced Ca2+ release. Inhibition of phospholipase C with U73122 did not change capsazepine-induced [Ca2+]i rises. Collectively, in MDCK cells, capsazepine induced [Ca2+]i rises by causing phospholipase C-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via non-L-type Ca2+ channels.

Original languageEnglish
Pages (from-to)323-329
Number of pages7
JournalDrug Development Research
Issue number4
StatePublished - 06 2011
Externally publishedYes


  • Ca
  • MDCK cells
  • capsazepine
  • fura-2
  • thapsigargin


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