Nonselective cation currents regulate membrane potential of rabbit coronary arterial cell: modulation by lysophosphatidylcholine.
BACKGROUND
The effects of lysophosphatidylcholine (LPC) on electrophysiological activities and intracellular Ca2+ concentration ([Ca2+]i) were investigated in coronary arterial smooth muscle cells (CASMCs).


RESULTS
The patch clamp techniques and Ca2+ measurements were applied to cultured rabbit CASMCs. The membrane potential was -46.0+/-5.0 mV, and LPC depolarized it. Replacement of extracellular Na+ with NMDG+ hyperpolarized the membrane and antagonized the depolarizing effects of LPC. In Na+-, K+-, or Cs+-containing solution, the voltage-independent background current with reversal potential (E(r)) of approximately +0 mV was observed. Removal of Cl- failed to affect it. When extracellular cations were replaced by NMDG+, E(r) was shifted to negative potentials. La3+ and Gd3+ abolished the background current, but nicardipine and verapamil did not inhibit it. In Na+-containing solution, LPC induced a voltage-independent current with E(r) of approximately +0 mV concentration-dependently. Similar current was recorded in K+- and Cs+-containing solution. La3+ and Gd3+ inhibited LPC-induced current, but nicardipine and verapamil did not inhibit it. In cell-attached configurations, single-channel activities with single-channel conductance of approximately 32pS were observed when patch pipettes were filled with LPC. LPC increased [Ca2+]i as the result of Ca2+ influx, and La3+ completely antagonized it.


CONCLUSIONS
These results suggest that (1) nonselective cation current (I(NSC)) contributes to form membrane potentials of CASMCs and (2) LPC activates I(NSC), resulting in an increase of [Ca2+]i. Thus, LPC may affect CASMC tone under various pathophysiological conditions such as ischemia.
Terasawa
Kuniko
K
Department of Cardiovascular Medicine, University of Tokyo, Tokyo, Japan.
Nakajima
Toshiaki
T
Iida
Haruko
H
Iwasawa
Kuniaki
K
Oonuma
Hitoshi
H
Jo
Taisuke
T
Morita
Toshihiro
T
Nakamura
Fumitaka
F
Fujimori
Yoshiharu
Y
Toyo-oka
Teruhiko
T
Nagai
Ryozo
R
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002478:Cells, Cultured; D002586:Cesium / Q000494:pharmacology; D003331:Coronary Vessels / Q000166:cytology*; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation / Q000379:methods; D005682:Gadolinium / Q000494:pharmacology; D007424:Intracellular Fluid / Q000378:metabolism; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D007811:Lanthanum / Q000494:pharmacology; D008244:Lysophosphatidylcholines / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D008536:Meglumine / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011817:Rabbits; D012964:Sodium / Q000378:metabolism
D002121:Calcium Channel Blockers; D007473:Ion Channels; D008244:Lysophosphatidylcholines; D026902:Potassium Channel Blockers; D002586:Cesium; D008536:Meglumine; D007811:Lanthanum; D012964:Sodium; D005682:Gadolinium; D011188:Potassium; D002118:Calcium