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Evidence for selective inhibition by lysophosphatidylcholine of acetylcholine‐induced endothelium‐dependent hyperpolarization and relaxation in rat mesenteric artery
Author(s) -
Fukao Mitsuhiro,
Hattori Yuichi,
Kanno Morio,
Sakuma Ichiro,
Kitabatake Akira
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb16370.x
Subject(s) - acetylcholine , hyperpolarization (physics) , lysophosphatidylcholine , endothelium , endothelium derived relaxing factor , chemistry , endothelium derived hyperpolarizing factor , nitric oxide , endocrinology , medicine , vasodilation , mesenteric arteries , biophysics , biology , biochemistry , artery , charybdotoxin , stereochemistry , phosphatidylcholine , nuclear magnetic resonance spectroscopy , phospholipid , membrane
The effects of lysophosphatidylcholine (LPC) on acetylcholine‐induced hyperpolarization and relaxation were examined in rat mesenteric arteries. LPC (3‐10 μ M ) reversibly inhibited endothelium‐dependent hyperpolarization by acetylcholine in a concentration‐dependent manner. LPC (10 μ M ) inhibited only partially endothelium‐dependent relaxation by acetylcholine. However, acetylcholine‐induced relaxation obtained in the presence of 100 μ M N G ‐nitro‐ L ‐arginine was almost completely eliminated by 10 μ LPC. These results indicate that LPC inhibits hyperpolarization and relaxation due to endothelium‐derived hyperpolarizing factor more specifically than the relaxation due to endothelium‐derived nitric oxide.