1. Nonselective cation currents regulate membrane potential of rabbit coronary arterial cell: modulation by lysophosphatidylcholine.
- Author
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Terasawa K, Nakajima T, Iida H, Iwasawa K, Oonuma H, Jo T, Morita T, Nakamura F, Fujimori Y, Toyo-oka T, and Nagai R
- Subjects
- Animals, Calcium metabolism, Calcium Channel Blockers pharmacology, Cells, Cultured, Cesium pharmacology, Dose-Response Relationship, Drug, Electric Stimulation methods, Gadolinium pharmacology, Intracellular Fluid metabolism, Ion Channels drug effects, Lanthanum pharmacology, Lysophosphatidylcholines pharmacology, Male, Meglumine pharmacology, Membrane Potentials drug effects, Muscle, Smooth, Vascular cytology, Muscle, Smooth, Vascular drug effects, Patch-Clamp Techniques, Potassium metabolism, Potassium Channel Blockers pharmacology, Rabbits, Sodium metabolism, Coronary Vessels cytology, Ion Channels metabolism, Lysophosphatidylcholines metabolism, Membrane Potentials physiology, Muscle, Smooth, Vascular metabolism
- Abstract
Background: The effects of lysophosphatidylcholine (LPC) on electrophysiological activities and intracellular Ca2+ concentration ([Ca2+]i) were investigated in coronary arterial smooth muscle cells (CASMCs)., Methods and 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.
- Published
- 2002
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