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on November 11, 2002

Circulation. 2002
Published online before print November 11, 2002, doi: 10.1161/01.CIR.0000039345.00481.1D
A more recent version of this article appeared on December 10, 2002
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Right arrow Ion channels/membrane transport

Submitted on June 24, 2002
Revised on August 29, 2002
Accepted on September 2, 2002

Nonselective Cation Currents Regulate Membrane Potential of Rabbit Coronary Arterial Cell. Modulation by Lysophosphatidylcholine

Kuniko Terasawa MD, Toshiaki Nakajima MD*, Haruko Iida MD, Kuniaki Iwasawa MD, Hitoshi Oonuma MD, Taisuke Jo MD, Toshihiro Morita MD, Fumitaka Nakamura MD, Yoshiharu Fujimori MD, Teruhiko Toyo-oka MD, and Ryozo Nagai MD

From the Department of Cardiovascular Medicine (K.T., T.N., H.I., K.I., H.O., T.J., T.M., F.N., T.T., R.N.), University of Tokyo, Tokyo, Japan; and the Department of Cardiology (K.T., Y.F.), Narita Red Cross Hospital, Chiba, Japan.

* To whom correspondence should be addressed. E-mail: masamasa{at}pb4.so-net.ne.jp.

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 (Er) of approximately +0 mV was observed. Removal of Cl- failed to affect it. When extracellular cations were replaced by NMDG+, Er 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 Er 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 {approx}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 (INSC) contributes to form membrane potentials of CASMCs and (2) LPC activates INSC, resulting in an increase of [Ca2+]i. Thus, LPC may affect CASMC tone under various pathophysiological conditions such as ischemia.


Key words: muscle, smooth • cells • ischemia • ion channels




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