Effect of lysophosphatidylcholine on whole cell K+ current in rabbit coronary smooth muscle cells..
10.4070/kcj.2001.31.2.217
- Author:
Chang Heon YI
;
Mi Young HA
;
Duck Sun AHN
;
Bok Soon KANG
- Publication Type:Original Article
- MeSH:
Arteries;
Constriction;
Coronary Vessels;
Lipoproteins;
Lysophosphatidylcholines*;
Muscle, Smooth*;
Myocytes, Smooth Muscle*;
Protein Kinase C;
Staurosporine;
Tea
- From:Korean Circulation Journal
2001;31(2):217-229
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Impairment of relaxing response and augmentation of contractile response to vasoactive substances have been reported in atherosclerotic arteries. These alterations in vascular reactivity are considered as an underlying mechanism for the development of acute vasospasm in atherosclerotic coronary artery. Recently, it has been reported that lysophophatidylcholine (LPC), an oxidative metabolite of low density lipoprotein causes this functional abnormality. However, the precise mechanism of LPC induced change of vascular reactivity is still uncertain. METHOD: In this study, to elucidate the underlying mechanisms of abnormal vascular reactivity in atherosclerotic coronary artery, we examined the effect of LPC on whole cell K+current using patch clamping technique in rabbit coronary smooth muscle cells. RESULTS: Application of LPC(1microM) showed dual effect on whole cell outward current which depends on the magnitude of test potentials. At relatively high depolarizing test potentials (> 10 mV), LPC increased amplitude of outward current which was blocked by Gd3+ not by iberiotoxin (100 nM) and TEA (1 mM). Reversal potential of this Gd3+sensitive, LPC-induced current was -9.7 +/- 0.6 mV. At less depolarizing test potentials (< 10 mV), LPC decreased whole cell K+currents in a dose dependent manner (from 0.01 to 10 microM) in the range of -30 mV to +0 mV. Half maximal inhibition of K+current was 1.509 microM at 0 mV test potential (n =5). Depolarizing holding potential (0 mV) prevented this LPC-induced inhibition of K+current. Steady state activation and inactivation parameters of K+current were significantly shifted to the positive direction by application of LPC (p < 0.01, n =8). Pretreatment of staurosporine (100 nM), a blocker of protein kinase C partially blocked LPC-induced decrease of K+currents. CONCLUSION: LPC-induced inhibition of voltage dependent K+current may explain abnormal vascular reactivity in atherosclerotic coronary artery.
