Secondary AV conduction responses during tonic vagal stimulation.

We gave trains of supramaximal stimuli at frequencies of 2, 4, or 8 Hz to both vagi of anesthetized, open-chest dogs and studied the AV conduction and atrial contractility responses while the atria were paced at different frequencies. The vagal stimulation quickly induced a maximum negative inotropic effect on the atrium. This "initial" response was followed by a "secondary" fading back toward the control level. The negative dromotropic responses to vagal stimulation also rapidly reached an initial value. When this initial response was large, there was then a secondary, relatively rapid fading back toward control. However, when the initial dromotropic response was small, the secondary response instead consisted of a gradual increase in conduction time. At intermediate levels of the initial dromotropic response, there was no appreciable secondary change in AV response. We hypothesize that two opposing mechanisms account for the variable secondary changes in AV conduction time and that the stimulus intensity determines which mechanism will be prepotent. The mechanism responsible for the secondary decline appears to be related to that which causes the fade of the inotropic response; muscarinic receptor desensitization probably plays an important role. The secondary augmentation of the dromotropic response may be related either to a slow diffusion of acetylcholine from the surrounding tissue or to a slow cumulative change in AV nodal refractoriness.