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Altered acetylcholine, bradykinin and cutaneous pressure‐induced vasodilation in mice lacking the TREK1 potassium channel: the endothelial link
Author(s) -
Garry Ambroise,
Fromy Bérengère,
Blondeau Nicolas,
Henrion Daniel,
Brau Frédéric,
Gou Pierre,
Guy Nicolas,
Heurteaux Catherine,
Lazdunski Michel,
Saumet Jean Louis
Publication year - 2007
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400916
Subject(s) - bradykinin , vasodilation , acetylcholine , endocrinology , medicine , mesenteric arteries , chemistry , potassium channel , endothelium , biology , receptor , artery
The TWIK related K + channel TREK1 is an important member of the class of two‐pore‐domain K + channels. It is a background K + channel and is regulated by hormones, neurotransmitters, intracellular pH and mechanical stretch. This work shows that TREK1 is present both in mesenteric resistance arteries and in skin microvessels. It is particularly well expressed in endothelial cells. Deletion of TREK1 in mice leads to an important alteration in vasodilation of mesenteric arteries induced by acetylcholine and bradykinin. Iontophoretic delivery of acetylcholine and bradykinin in the skin of TREK1 +/+ and TREK1 −/− mice also shows the important role of TREK1 in cutaneous endothelium‐dependent vasodilation. The vasodilator response to local pressure application is also markedly decreased in TREK1 −/− mice, mimicking the decreased response to pressure observed in diabetes. Deletion of TREK1 is associated with a marked alteration in the efficacy of the G‐protein‐coupled receptor‐associated cascade producing NO that leads to major endothelial dysfunction.