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In humane, the parasympathetic nervous system predominates over the sympathetic nervous system in control of heart rate, but little is known about the relative influences of cholinergic and adrenergic tone on the electrophysiological properties of the ventricle and atrioventricular (AV) node. Thirteen subjects were studied using standard electrophysiological testing techniques in the control state and after propranolol (0.15 mg/kg, iv) plus atropine (0.03 mg/kg, iv) to assess the effect of autonomic blockade on ventricular and AV nodal refractoriness and AV nodal conduction. Eight subjects received propranolol first (group A) and five were given atropine first (group B). For groups A and B, the spontaneous sinus cycle length significantly decreased from control after administration of propranolol and atropine [813 ± 107 (SD) to 613 ± 57 msec and 842 ± 188 to 637 ± 115 msec, respectively]. Ventricular effective (ERP) and functional (FRP) refractory periods insignificantly increased from control after propranolol was given (group A); however, both ventricular ERP and FRP significantly shortened to less than control values after atropine was added (238 ± 23 to 218 ± 19 msec and 261 ± 22 to 243 ± 17 msec, respectively). Similar results for ventricular refractoriness occurred after administration of atropine and propranolol in group B subjects. The shortest atrial pacing cycle length sustaining 1:1 AV nodal conduction after administration of propranolol and atropine did not significantly change from control values (386 ± 109 to 372 ± 74 msec). These data suggest that (1) resting vagal tone exerts a significant effect on human ventricular refractoriness and the effect can occur in the presence of β-adrenergic blockade, and (2) in contrast to the markedly predominant effect of the parasympathetic nervous system on sinus nodal automaticity, vagal and adrenergic tone exert a balanced effect on resting AV nodal conduction.

circulation research

Effect of autonomic blockade on ventricular refractoriness and atrioventricular nodal conduction in humans. Evidence supporting a direct cholinergic action on ventricular muscle refractoriness.