AJP - Heart and Circulatory Physiology, Vol 271, Issue 3 870-H875, Copyright © 1996 by American Physiological Society
Reflex vagal control of atrial repolarization
D. E. Euler, B. Olshansky and S. Y. Kim
Department of Medicine, Loyola University Medical Center, Maywood, Illinois 60153, USA.
The reflex vagal control of atrial repolarization was investigated in eight
open-chest, anesthetized dogs. A monophasic action potential was recorded
from the right atrium, and the action potential duration to 90%
repolarization (APD90) was determined every cardiac cycle. beta-Adrenergic
receptors were blocked with timolol (0.1 mg/kg). Under baseline conditions,
sinus slowing during sinus arrhythmia was accompanied by a significant
shortening of APD90 (24 +/- 4.0 ms). Transient occlusion (30 s) of the
descending thoracic aorta increased systolic aortic pressure from 138 +/-
2.8 to 181 +/- 3.3 mmHg (P < 0.01). Heart rate decreased from 99 +/- 3.6
to 42.5 +/- 3.4 beats/min (P < 0.01), and APD90 shortened from 168 +/-
5.1 to 94 +/- 3.3 ms (P < 0.01). Release of the occlusion caused
arterial hypotension (95 +/- 2.8 mmHg) and an overshoot in both rate (126
+/- 5.2 beats/min) and APD90 (189 +/- 2.3 ms). Aortic occlusion during
atrial pacing (130-160 beats/min) decreased APD90 from 147 +/- 7.0 to 78
+/- 3.4 ms (P < 0.01). Cervical vagotomy or atropine eliminated changes
in rate and APD90 evoked by aortic occlusion. The results indicate that
there is parallel central vagal control of both sinus rate and atrial
repolarization. Sinus bradycardia during reflex vagal activation does not
prevent the acceleration of atrial repolarization.
