Experiments were conducted using 108 dogs to study dependence of the sinus node and atrioventricular (A V) junction on adrenergic neural tone. The sinus node was selectively suppressed by direct perfusion of physostigmine (100 μg/ml) through its nutrient artery, with consistent production of a stable A V junctional escape rhythm. The 3 procedures used to impair adrenergic neural influence were bilateral stellectomy and upper thoracic sympathectomy; selective blockade of adrenergic beta receptors in the sinus node or A V junction by direct perfusion of propranolol (10 and 100 μg/ml); and pretreatment with reserpine, 0.5 mg/kg i.m., for 2 days prior to study. Although both escape time and rate of escape rhythm were impaired by interrupting adrenergic neural influence in either the sinus node or A V junction, the effect on the latter was more pronounced. Selective beta receptor blockade slowed sinus rhythm 19% but slowed A V junctional rhythm 43%. Furthermore, A V junctional escape after interruption of adrenergic neural tone was marked by periods of asystole or slow erratic beats for as long as 1 min or more. No stable subjunctional escape rhythm was observed in any experiment. Both the 2 normal automatic centers in the heart are dependent on adrenergic neural tone, but the A V junction more than the sinus node.
