Role of chloride currents in repolarizing rabbit atrial myocytes. Wang, Zhiguo, Bernard Fermini, Jianlin Feng, and Stanley Nattel. Department of Medicine, Montreal Heart Institute and University of Montreal, Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada H1T 1C8
APStracts 2:0004H, 1995.
Rabbit atrial cells manifest a prominent transient outward K+ current (Ito1) but this current recovers slowly from inactivation and is unlikely to be important at physiologic rates (3-5 Hz). Depolarization of rabbit atrial cells also elicits a transient calcium-dependent outward Cl- current (Ito2). To compare the relative magnitude of these transient outward currents at various rates, we applied whole-cell voltage clamp techniques to isolated rabbit atrial myocytes. While peak Ito1 exceeded Ito2 at slow rates (0.1 Hz), Ito1 was strongly reduced as rate was increased (by 97 +/- 2%, mean +/- SE, at 4 Hz), while Ito2 was slightly reduced (by 28 +/- 4%, 4 Hz). The reversal potential of transient outward tail currents at 0.07 Hz was -49 +/- 9 mV, while at 2.5 Hz the reversal potential became -18 +/- 7 mV (calculated Cl- reversal potential -18 mV). The addition of the Cl- transport blocker DIDS (150 [mu]M) or the replacement of external Cl- with methanesulfonate inhibited a large part of the transient outward current elicited by depolarization at 4 Hz. DIDS and Cl- replacement increased action potential duration in both single rabbit atrial cells and multicellular rabbit atrial preparations. We conclude that the Ca2+-dependent Cl- current is substantially larger than the transient K+ current at physiologic rates in the rabbit, and is likely to play a more important role in action potential repolarization than the latter current in this tissue in vivo.

Received 7 June 1993; accepted in final form 4 January 1995.
APS Manuscript Number H0491-3.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 February 1995.