Reflex vagal control of atrial repolarization.

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 (APD 90 ) was determined every cardiac cycle. β-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 APD 90 (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 APD 90 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 APD 90 (189 ± 2.3 ms). Aortic occlusion during atrial pacing (130-160 beats/min) decreased APD 90 from 147 ± 7.0 to 78 ± 3.4 ms (P < 0.01). Cervical vagotomy or atropine eliminated changes in rate and APD 90 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.