Menon N K, Bing R J
Huntington Medical Research Institutes, Department of Experimental Cardiology, Pasadena, CA 91105.
Proc Soc Exp Biol Med. 1991 Apr;196(4):461-3. doi: 10.3181/00379727-196-4-rc1.
Lysophosphatidylcholine (LPC) is a potent endothelium-dependent vascular smooth muscle relaxant. The possibility that its action is mediated through endothelium-derived nitric oxide (EDNO), although suggestive, has not been proven. Both lysophosphatidylcholine and endothelium-derived nitric oxide relax by activating guanylate cyclase to form cyclic GMP. Based on the finding that EDNO formation is inhibited by NNA (N-omega-nitro-L-arginine), we followed cyclic GMP changes in bovine intrapulmonary arteries with LPC after incubation with NNA. Inhibition of cyclic GMP by LPC following NNA exposure would be suggestive of the production of EDNO by LPC. However, while NNA significantly inhibited accumulation of cyclic GMP after exposure to the calcium ionophore A23187 which releases EDNO, NNA failed to inhibit LPC-induced accumulation of cyclic GMP. The results indicate that LPC relaxes vascular smooth muscle through a non NO-mediated pathway.
溶血磷脂酰胆碱（LPC）是一种强效的内皮依赖性血管平滑肌舒张剂。其作用通过内皮衍生的一氧化氮（EDNO）介导的可能性虽然有提示作用，但尚未得到证实。溶血磷脂酰胆碱和内皮衍生的一氧化氮都通过激活鸟苷酸环化酶形成环磷鸟苷（cGMP）来实现舒张。基于N-ω-硝基-L-精氨酸（NNA）抑制EDNO形成这一发现，我们在NNA孵育后观察了牛肺内动脉中LPC作用下的cGMP变化。NNA暴露后LPC对cGMP的抑制作用将提示LPC产生了EDNO。然而，虽然NNA在暴露于释放EDNO的钙离子载体A23187后显著抑制了cGMP的积累，但NNA未能抑制LPC诱导的cGMP积累。结果表明，LPC通过非NO介导的途径使血管平滑肌舒张。
