The electrophysiological properties of N-allyl-clonidine (ST 567) were studied in 18 patients. Four of these patients were pretreated with intravenous propranolol, 0.2 mg/kg, and atropine, 0.04 mg/kg, to induce autonomic blockade. ST 567 produces a sustained bradycardiac effect at a dose of 40 mg, i.v., in patients without (group I) and with (group II) autonomic blockade. The mean increase in Group I was 23% and in group II, 42%. The sinus node recovery time increased in both groups, from 1,151 +/- 73 to 1,310 +/- 81 msec in group I, and from 995 +/- 145 to 1,599 +/- 248 msec (means +/- SEM) in group II. The corrected sinus node recovery time was unaffected by ST 567 in Group I and increased from 165 +/- 50 to 427 +/- 117 msec in group II. The sinoatrial conduction time was unaffected by ST 567 in group I. The effective refractory period of the right atrium, the atrioventricular node and the right ventricle, as well as the functional refractory period of the atrioventricular node, were unaffected by ST 567 in patients without autonomic blockade. Intra-atrial, atrioventricular, and intraventricular conduction were also not altered by this drug. Thus, the electrophysiological profile of ST 567 differs from other bradycardia-inducing agents such as beta-blockers or calcium antagonists.