ID 111546
Author
Harada, Nagakatsu The University of Tokushima KAKEN Search Researchers
Content Type
Journal Article
Description
In vascular smooth muscle cells, large-conductance Ca2+-activated K+ channels (KCa channels) play a pivotal role in determining membrane potential, and thereby the vascular tone. Ginsenoside Re, a phytochemical from ginseng, is reported to activate this channel, but its precise mechanism is unsolved. Patch clamp studies showed that ginsenoside Re activates KCa channels in the arterial smooth muscle cell line A10 in a dose-dependent manner. The channel-opening effect of ginsenoside Re was inhibited by 1 μM L-NIO, an inhibitor of eNOS, but not by 3 μM SMTC, an inhibitor of nNOS, indicating that ginsenoside Re activated KCa channels through activation of eNOS. SH-6 (10 μM), an Akt inhibitor, and wortmannin, a PI3-kinase inhibitor, completely blocked activation of KCa channels by ginsenoside Re, indicating that it activates eNOS via a c-Src/PI3-kinase/ Akt-dependent mechanism. In addition, the ginsenoside Re-induced activation of eNOS and KCa channel was blocked by 10 μM ICI 182,780, an inhibitor of membrane estrogen receptor-α, suggesting that eNOS activation occurs via a non-genomic pathway of this receptor. In conclusion, ginsenoside Re releases NO via a membrane sex steroid receptors, resulting in KCa channel activation in vascular smooth muscle cells, promoting vasodilation and preventing severe arterial contraction.
Journal Title
The Journal of Medical Investigation
ISSN
13496867
13431420
NCID
AA11166929
AA12022913
Publisher
Faculty of Medicine Tokushima University
Volume
54
Issue
3-4
Start Page
381
End Page
384
Sort Key
381
Published Date
2007-08
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Medical Sciences
University Hospital