Fukao M, Hattori Y, Kanno M, Sakuma I, Kitabatake A
Department of Pharmacology, Hokkaido University School of Medicine, Sapporo, Japan.
Br J Pharmacol. 1995 Sep;116(1):1541-3. doi: 10.1111/j.1476-5381.1995.tb16370.x.
The effects of lysophosphatidylcholine (LPC) on acetylcholine-induced hyperpolarization and relaxation were examined in rat mesenteric arteries. LPC (3-10 microM) reversibly inhibited endothelium-dependent hyperpolarization by acetylcholine in a concentration-dependent manner. LPC (10 microM) inhibited only partially endothelium-dependent relaxation by acetylcholine. However, acetylcholine-induced relaxation obtained in the presence of 100 microM NG-nitro-L-arginine was almost completely eliminated by 10 microM 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.
在大鼠肠系膜动脉中研究了溶血磷脂酰胆碱（LPC）对乙酰胆碱诱导的超极化和舒张的影响。LPC（3 - 10微摩尔）以浓度依赖的方式可逆地抑制乙酰胆碱引起的内皮依赖性超极化。LPC（10微摩尔）仅部分抑制乙酰胆碱引起的内皮依赖性舒张。然而，在存在100微摩尔NG-硝基-L-精氨酸的情况下获得的乙酰胆碱诱导的舒张几乎被10微摩尔LPC完全消除。这些结果表明，LPC对内皮源性超极化因子引起的超极化和舒张的抑制作用比内皮源性一氧化氮引起的舒张更具特异性。
