Lysophosphatidylcholine Inhibits Relaxation of Rabbit Abdominal Aorta Mediated by Endothelium-Derived Nitric Oxide and Endothelium-Derived Hyperpolarizing Factor Independent of Protein Kinase C Activation

Abstract Hypercholesterolemia is associated with increased oxidized LDL and impaired endothelium-dependent relaxation (EDR). An inhibitory component of oxidized LDL is lysophosphatidylcholine (LPC). To determine the effect and mechanism(s) of action of LPC on EDR mediated by endothelium-derived nitric oxide (EDNO) and endothelium-derived hyperpolarizing factor (EDHF), rabbit abdominal aortic rings were suspended for measurement of isometric tension and studied under three conditions: control; with 25 mmol/L K+ buffer to isolate relaxation mediated by EDNO; and in rings treated with Nω-nitro-l-arginine methyl ester (L-NAME, 30 μmol/L) to isolate relaxation mediated by EDHF. Incubation with LPC (10 and 30 μmol/L) for 30 minutes inhibited EDR in a concentration-dependent manner. LPC (30 μmol/L) significantly inhibited maximal relaxation to acetylcholine in control, 25 mmol/L K+–, and L-NAME–treated rings (77.1±7.8%, 42.1±8.9%, and 3.4±7.7%) compared with untreated rings (99.0±0.9%, 90.9±2.2%, and 54.7±4.7%, ...