Nonselective Cation Currents Regulate Membrane Potential of Rabbit Coronary Arterial Cell

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Abstract
Background— The effects of lysophosphatidylcholine (LPC) on electrophysiological activities and intracellular Ca 2+ concentration ([Ca 2+ ] i ) were investigated in coronary arterial smooth muscle cells (CASMCs). Methods and Results— The patch clamp techniques and Ca 2+ 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. La 3+ and Gd 3+ 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. La 3+ and Gd 3+ inhibited LPC-induced current, but nicardipine and verapamil did not inhibit it. In cell-attached configurations, single-channel activities with single-channel conductance of ≈32pS were observed when patch pipettes were filled with LPC. LPC increased [Ca 2+ ] i as the result of Ca 2+ influx, and La 3+ 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 [Ca 2+ ] i . Thus, LPC may affect CASMC tone under various pathophysiological conditions such as ischemia.