14th International Congress
THE "NEW FRONTIERS"
OF ARRHYTHMIAS 2000

Jan. 29 - Feb. 5, 2000
Marilleva, Trento, Italy

RT-33

Arrhythmogenic mechanisms of norepinephrine in depolarized single ventricular myocytes

Yejia Song, Mario Vassalle.
Department of Physiology and Pharmacology, State University of New York, Health Science Center, New York, USA

Abstract

BACKGROUND. The induction of spontaneous activity by norepinephrine (NE) in depolarized myocardial cells and its mechanism were studied in ventricular myocyte isolated from guinea pig heart.

METHODS AND RESULTS. Membrane potentials and current were recorded by means of a single electrode voltage clamp method. Depolarization of ventricular myocytes by current passed through the recording microelectrode induced diastolic depolarization in many but not in all cells. In depolarized myocytes, NE increased the amplitude and duration of the action potential and increased the slope and amplitude of the depolarization-induced pacemaker potential. NE also induced oscillatory potentials (V_os) which often attained the threshold and caused fast spontaneous activity. In voltage-clamped myocytes, NE increased the slow inward current and slowed its decay, and induced an oscillatory current that peaked at depolarized levels and could initiate repetitive regenerative currents. NE induced voltage-dependent V_os and spontaneous activity also in those myocytes that did not develop DD on depolarization. Acetylcholine reduced or suppressed the NE-induced spontaneous discharge.

CONCLUSION. The combination of increased calcium influx by NE and of increased V_os size by depolarization appears to be the mechanism by which fast spontaneous discharge is initiated by NE in depolarized myocardial cells.

Key Words