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Lysophosphatidylcholine Decreases Delayed Rectifier K+ Current in Rabbit Coronary Smooth Muscle Cells

 Dongsoo YEON  ;  Seongchun KWON  ;  Taicksang NAM  ;  Ducksun AHN 
 Journal of Veterinary Medical Science, Vol.63(4) : 395-399, 2001 
Journal Title
 Journal of Veterinary Medical Science 
Issue Date
Animals ; Coronary Vessels/cytology ; Coronary Vessels/drug effects ; Coronary Vessels/physiology ; Drug Antagonism ; Enzyme Inhibitors ; Lysophosphatidylcholines/antagonists & inhibitors ; Lysophosphatidylcholines/pharmacology* ; Membrane Potentials/drug effects ; Membrane Potentials/physiology ; Muscle, Smooth, Vascular/drug effects* ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/physiology ; Patch-Clamp Techniques ; Peptides/pharmacology ; Potassium Channel Blockers* ; Potassium Channels/physiology ; Protein Kinase C/physiology ; Rabbits ; Staurosporine/pharmacology
coronary smooth muscle ; delayed rectifier K+ current ; lysophosphatidylcholine ; protein kinase C
Lysophosphatidylcholine (LPC), which exists abundantly in lipid fraction of oxidized low density lipoprotein, has been implicated in enhanced agonist-induced contraction and increase of intracellular Ca2+. The effect of LPC on the activity of delayed rectifier K+ current (IdK), which is a major determinant of membrane potential and vascular tone under resting condition, was examined in rabbit coronary smooth muscle cells using whole cell patch clamping technique. Application of LPC to the bath solution caused a concentration-dependent inhibition of IdK, and the concentration to produce half-maximal inhibition was 1.51 μM. This effect of LPC on IdK was readily reversed after washout of LPC in the bath. The steady-state voltage dependence of IdK was shifted to positive direction by both extra- and intracellular application of LPC. Staurosporine (100 nM) pretreatment significantly suppressed the LPC-induced inhibition of IdK. These results suggest that LPC inhibits IdK in rabbit coronary smooth muscle cells by a pathway that involves protein kinase C, and the LPC-induced inhibition of IdK may be, at least in part, responsible for the abnormal vascular reactivity in atherosclerotic coronary artery.
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1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Nam, Taick Sang(남택상)
Ahn, Duk Sun(안덕선) ORCID logo https://orcid.org/0000-0001-9351-6951
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