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Cardiovascular Research 1999 43(4):901-908; doi:10.1016/S0008-6363(99)00124-8
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Differences in the electrophysiologic response of four canine ventricular cell types to {alpha}1-adrenergic agonists

Alexander Burashnikov and Charles Antzelevitch*

Masonic Medical Research Laboratory, 2150 Bleecker Street, Utica, NY 13501, USA

* Corresponding author. Tel.: +1-315-735 2217; fax: +1-315-735 5648 CA{at}mmrl.edu

Objective: The present study was designed to examine regional differences in the response of {alpha}1 adrenoceptor stimulation in the canine ventricle. Methods: Standard microelectrode techniques were used to record transmembrane action potentials from epicardial, M cell, and endocardial as well as Purkinje fiber preparations isolated from the canine left ventricle. Results: Phenylephrine (0.1–10 µM+propranolol 0.2 µM) and methoxamine (1–10 µM) produced dose- and rate-dependent prolongation of action potential duration (APD90) in Purkinje fibers (P<0.05, at 0.1–10 µM, BCL=0.5–2 s), but an abbreviation of APD90 in tissues from the M region (P<0.05, at 10 µM, BCL=0.5–2 s). At slow pacing rates (≥2 s), phenylephrine (1 µM) exerted a small, significant (P<0.05) prolongation of APD90 in epicardium and endocardium which returned to control values when the concentration was increased to 10 µM. The amplitude of phase 1 of the action potential in M and epicardial cells was significantly increased by phenylephrine at concentrations of 10 µM (P<0.05). Prazosin (1 µM), a nonspecific {alpha}1 antagonist, reversed these effects of phenylephrine (10 µM) and methoxamine (10 µM) on APD90 and the action potential notch. The {alpha}1b-antagonist, chloroethylclonidine (0.1–1.0 µM), but not the {alpha}1a-antagonist, WB-4101 (0.1–1.0 µM), reversed the APD-abbreviating effect of methoxamine in the M cell. Conclusion: Our results demonstrate striking regional differences in the electrophysiological response of the four canine ventricular cell types to {alpha}1 adrenergic agonists. Our data provide support for the hypothesis that different adrenoceptor subtypes underlie the opposite response of M cells ({alpha}1b-APD abbreviation) and Purkinje fibers ({alpha}1a-APD prolongation) to {alpha}1-adrenoceptor activation.

KEYWORDS Experimental; Heart; Electrophysiology; Adrenergic agonists; Autonomic nervous system; Canine; M cell; Purkinje fiber


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