A protein kinase G-sensitive channel mediates flow-induced Ca2+ entry into vascular endothelial cells

Xiaoqiang Yao*, Hiu Yee Kwan, Franky Leung Chan, Nickie Wai Kei Chan, Yu Huang

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

54 Citations (Scopus)


The hemodynamic force generated by blood flow is considered to be the physiologically most important stimulus for the release of nitric oxide (NO) and prostacyclin (PGI2) from vascular endothelial cells (1). NO and PGI2 then act on the underlying smooth muscle cells, causing vasodilation and thus lowering blood pressure (2, 3). One critical early event occurring in this flow-induced regulation of vascular tone is that blood flow induces Ca2+ entry into vascular endothelial cells, which in turn leads to the formation of NO (4, 5). Here we report a mechanosensitive Ca2+-permeable channel in vascular endothelial cells. The activity of the channel was inhibited by 8- Br-cGMP, a membrane-permeant activator of protein kinase G (PKG), in cell- attached membrane patches. The inhibition could be reversed by PKG inhibitor KT5823 or H-8. A direct application of active PKG in inside-out patches blocked the channel activity. Gd3+, Ni2+, or SK and F-96365 also inhibited the channel activity. A study of fluorescent Ca2+ entry revealed a striking pharmacological similarity between the Ca2+ entry elicited by flow and the mechanosensitive Ca2+-permeable channel we identified, suggesting that this channel is the primary pathway mediating flow-induced Ca2+ entry into vascular endothelial cells.

Original languageEnglish
Pages (from-to)932-938
Number of pages7
JournalFASEB Journal
Issue number7
Publication statusPublished - May 2000

Scopus Subject Areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

User-Defined Keywords

  • Blood flow
  • Endothelium
  • Nonselective cation channel
  • Shear stress


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