Interrelationship of Potassium and Vagal Action on the Sinoatrial Pacemaker and on Atrioventricular Conduction*

In a previous communication, evidence was presented that elevation of plasma potassium from a mean control level of 3.4 mEq per L to a mean of 6.1 mEq per L inhibited or greatly reduced the ability of acetylcholine to induce atrioventricular (AV) block (1). These observations were made utilizing intermittent intracoronary injections of acetylcholine and intravenous infusion of potassium. The purpose of the present investigation was threefold: first, to study the interaction between potassium and endogenously liberated acetylcholine (vagal action) rather than exogenous acetylcholine as had been done previously; second, to determine if this interrelationship applies equally to AV transmission and impulse formation by the sinoatrial (SA) node; third, to eliminate by direct intracoronary injection of potassium the possibility that the results in the initial study were due to the peripheral effects of the cation. Methods Thirteen experiments were performed on twelve mongrel dogs weighing from 10.7 to 16.5 kg. The animals were anesthetized with intramuscular morphine, 2.5 mg per kg, followed in 30 minutes by intravenous pentobarbital, 15 mg per kg. The dogs were intubated, and ventilation was controlled with a Harvard respirator. The ventilatory rate varied between 14 and 20 breaths per min-* Submitted for publication June 26, 1964; accepted