Pathways of [Ca2+]i rise evoked by angiotensin II in MDCK renal tubular cells

Chung Pin Liu, Chiang Ting Chou, Wei Zhe Liang, Jin Shiung Cheng, Hong Tai Chang, Daih Huang Kuo, Kuang Chung Ko, Ni Na Chiang, Ru Fang Wu, Pochuen Shieh, Chung Ren Jan*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

4 Scopus citations


The effect of angiotensin II (Ang II) on cytosolic Ca2+ concentrations ([Ca2+]i) in MDCK renal tubular cells was explored. The Ca2+-sensitive fluorescent dye fura-2 was applied to measure [Ca2+]i. Ang II at concentrations of 5-40 M induced a [Ca 2+]i rise in a concentration-dependent manner. The response was reduced partly by removing Ca2+. Ang II evoked store-operated Ca 2+ entry that was inhibited by La3+ and Gd3+. In the absence of extracellular Ca2+, incubation with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) or thapsigargin abolished Ang II-induced Ca2+ release. Inhibition of phospholipase C with U73122 abolished Ang II-induced [Ca2+]i rise. Three Ang II analogues [(ASN1,VAL5)-Ang II acetate, (SAR1,THR8)-Ang II acetate, (VAL5)-Ang II acetate] failed to induce a [Ca2+]i rise. Together, in MDCK cells, Ang II induced a [Ca2+]i rise via Ca2+ entry through store-operated Ca2+ channels and phospholipase C-dependent Ca2+ release from the endoplasmic reticulum. Moreover, Ang II's amino acid sequence is important in its stimulatory effect on [Ca2+]i.

Original languageEnglish
Pages (from-to)380-386
Number of pages7
JournalJournal of Receptors and Signal Transduction
Issue number6
StatePublished - 12 2013
Externally publishedYes


  • Ang II
  • Ca
  • MDCK
  • Renal cells


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