cGMP abolishes agonist-induced [Ca2+]i oscillations in human bladder epithelial cells

Hiu Yee Kwan, Yu Huang, Siu Kai Kong, Xiaoqiang Yao*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

5 Citations (Scopus)


Cytosolic calcium oscillations may permit cells to respond to information provided by increases in intracellular Ca2+ concentration ([Ca2+]i) while avoiding prolonged exposure to constantly elevated [Ca2+]i. In this study, we demonstrated that agonists could induce Ca2+ oscillations in human bladder epithelial cells. Application of 10 μM acetylcholine or 200 nM bradykinin triggered an initial Ca2+ transient that was followed by periodic [Ca2+]i oscillations. The oscillations did not depend on extracellular Ca2+. 8-Bromoguanosine 3′,5′-cyclic monophosphate abolished acetylcholine- or bradykinin-induced oscillations. Elevation of cellular cGMP by dipyridamole, an inhibitor of cGMP-specific phosphodiesterase, also terminated the [Ca2+]i oscillations. The inhibitory effect of cGMP could be reversed by KT-5823, a highly specific inhibitor of protein kinase G (PKG), suggesting that the action of cGMP was mediated by PKG. Comparison of the effect of cGMP with that of xestospongin C, an inhibitor of the inositol 1,4,5-trisphosphate (IP3) receptor, revealed similarities between the action of cGMP and xestospongin C. Therefore, it is likely that cGMP and PKG may target a signal transduction step(s) linked to IP3 receptor-mediated Ca2+ release.

Original languageEnglish
Pages (from-to)F1067-F1074
Number of pages8
JournalAmerican Journal of Physiology - Renal Physiology
Issue number6
Publication statusPublished - Dec 2001

Scopus Subject Areas

  • Physiology
  • Urology

User-Defined Keywords

  • Calcium release
  • Guanosine 3′,5′-cyclic monophosphate
  • Inositol 1,4,5-triphosphate
  • Intracellular calcium concentration
  • Nitric oxide
  • Protein kinase G


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