We hypothesized that a brief burst of vagal stimulation applied in each cardiac cycle could elicit an atrioventricular (AV) nodal Wenckebach arrhythmia. Twenty-six dogs were anesthetized with pentobarbital sodium (30 mg/kg iv) and were given propranolol (1 mg/kg iv). We varied the timing of a vagal stimulus burst in steps of 25-50 ms relative to the onset of atrial or ventricular depolarization. In four of nine experiments, a Wenckebach arrhythmia occurred despite changing the timing of stimuli. By prolonging the effects of vagal stimulation on AV conduction with physostigmine, the timing of the stimuli no longer influenced the severity of the arrhythmia. We did experiments to open one of the feedback control loops; these results indicated that this arrhythmia has elements of a positive feedback control system. We also studied the effects of vagal stimulation on the arrhythmia during retrograde conduction. We found that the timing of vagal stimulation was critical in eliciting the arrhythmia in only 4 of the 10 dogs.