Lysophosphatidylcholine Attenuates Endothelium-dependent Relaxation Responses through Inhibition of ACh-induced Endothelial Ca2+i Increase.
- Author:
Seong Chun KWON
1
;
Yong Ho LEE
;
Taicksang NAM
;
Duck Sun AHN
Author Information
1. Department of Physiology, College of Medicine, Kwandong University, Gangneung 210-701, Korea.
- Publication Type:Original Article
- Keywords:
Vascular endothelium;
LPC;
EDR;
Endothelial [Ca2+]i
- MeSH:
Acetylcholine;
Arteries;
Carotid Arteries;
Cytosol;
Endothelial Cells;
Endothelium;
Endothelium, Vascular;
Hand;
Lysophosphatidylcholines*;
NG-Nitroarginine Methyl Ester;
Relaxation*
- From:The Korean Journal of Physiology and Pharmacology
2006;10(1):25-30
- CountryRepublic of Korea
- Language:English
-
Abstract:
Lysophosphatidylcholine (LPC), which accumulates in atherosclerotic arteries, has been reported to inhibit endothelium-dependent relaxation (EDR) in many different species. However, the underlying mechanism of LPC-induced inhibition of EDR is still uncertain. In the present study, we measured simultaneously both isometric tension and cytosolic free Ca2+ ([Ca2+]i) in rabbit carotid strips, and examined the effect of LPC on tension and [Ca2+]i. In carotid strips with intact-endothelium, high K+ (70 mM) increased both tension and [Ca2+]i, and cumulative addition of acetylcholine (ACh) from 0.1 to 10microM induced dose dependent increase of [Ca2+]i with concomitant relaxation. In the presence of L-NAME (0.1 mM), ACh increased [Ca2+]i without affecting the amplitude of high K+-induced tension. These ACh-induced change of [Ca2+]i and tension was abolished by removal of endothelium or 10 nM 4-DAMP (muscarinic receptor antagonist) pretreatment. Pretreatment of LPC (10microM) inhibited ACh (10microM)-induced change of tension and [Ca2+]i in endothelium-intact carotid artery. On the other hand, LPC had no effect on ACh-induced change of tension and [Ca2+]i in endothelium denuded artery. In Ca2+-free external solution, ACh transiently increased [Ca2+]i, and pretreatment of LPC significantly inhibited ACh-induced transient [Ca2+]i change. Based on the above results, it may be concluded that LPC inhibits the ACh-induced [Ca2+]i change through inhibition of Ca2+ mobilization in vascular endothelial cells, resulting in decreased production of NO and concomitant inhibition of endothelium-dependent vascular relaxation.
