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. beta- Adrenergic receptors were blocked with timolol (0.1 mg/kg). Under base line conditions, sinus slowing during sinus arrhythmia was accompanied by a significant shortening of APD(90) (24 +/- 4.0 ms). Transient occ lusion (30 s) of the descending thoracic aorta increased systolic aort ic pressure from 138 +/- 2.8 to 181 +/- 3.3 mmHg (P < 0.01). Heart rat e 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). Releas e of the occlusion caused arterial hypotension (95 +/- 2.8 mmHg) and a n 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) dec reased 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 brad ycardia during reflex vagal activation does not prevent the accelerati on of atrial repolarization.