Lysophosphatidylcholine Inhibits Receptor-Mediated Ca2+ Mobilization in Intact Endothelial Cells of Rabbit Aorta

• Published in: Arteriosclerosis, thrombosis, and vascular biology Vol. 17; no. 8; pp. 1561 - 1567
• Main Authors: Miwa, Yoichi, Hirata, Ken-ichi, Kawashima, Seinosuke, Akita, Hozuka, Yokoyama, Mitsuhiro
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01-08-1997; Hagerstown, MD Lippincott
• Subjects: Acetylcholine - pharmacology; Animals; Aorta, Thoracic - cytology; Biological and medical sciences; Blood vessels and receptors; Calcium - metabolism; Cattle; Endothelium, Vascular - chemistry; Endothelium, Vascular - cytology; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Lysophosphatidylcholines - pharmacology; Muscle Relaxation - drug effects; Muscle, Smooth, Vascular - cytology; Nitric Oxide - physiology; Nitroglycerin - pharmacology; Phospholipids - pharmacology; Rabbits; Receptors, Cell Surface - antagonists & inhibitors; Receptors, Cell Surface - physiology; Vertebrates: cardiovascular system; Endothelial cell; Calcium; Rabbit; Exploration; Lagomorpha; Lysophosphatidylcholine; Mobilization; Vertebrata; Mammalia; Animal; Aorta; Circulatory system; Inhibition; Intracellular; Biological receptor
• ISSN: 1079-5642; 1524-4636
• DOI: 10.1161/01.atv.17.8.1561

We have previously reported that lysophosphatidylcholine (LPC), which accumulates in oxidized LDL and atherosclerotic arteries, inhibits endothelium-dependent relaxation and modulates Ca regulation in cultured bovine aortic endothelial cells. To test the effect of LPC on endothelium-dependent relaxation and endothelial Ca regulation in intact vessels, we simultaneously measured both isometric tension and endothelial cytosolic free Ca concentration ([Ca]i), using fura 2, in intact endothelial cells of aortic strips isolated from rabbits. In the aortic strips precontracted with phenylephrine, cumulative addition of acetylcholine (ACh) dose dependently induced endothelium-dependent relaxation, with an increase in endothelial [Ca]i, and positive correlation was obtained between these two parameters. LPC (2 to 20 micro mol/L) inhibited both ACh (3 micro mol/L)-induced endothelium-dependent relaxation and an increase in endothelial [Ca]i in a dose-dependent manner. On the other hand, phosphatidylcholine (20 micro mol/L) affected neither ACh-induced endothelium-dependent relaxation nor an increase in endothelial [Ca]i. LPC had no effect on endothelium-independent relaxation and a decrease in smooth muscle [Ca]i induced by nitroglycerin. Thus, the inhibitory effect of LPC on endothelium-dependent relaxation is due to the inhibition of agonist-induced Ca mobilization in vascular endothelial cells, which is an essential step in the synthesis of endothelium-derived relaxing factor. (Arterioscler Thromb Vasc Biol. 1997;17:1561-1567.)