Lack of a direct effect of efferent cardiac vagal nerve activity on atrial receptor activity.

Experiments were carried out to determine the extent to which the efferent cardiac vagus may modulate the discharge from atrial receptors when heart rate was not controlled. Stimulation of the vagus increased atrial pressure and the discharge from type-B atrial receptors. In order to determine the extent to which the increase in atrial receptor discharge was the result of the associated hemodynamic changes, studies were done in which the vagus was stimulated while heart rate was maintained constant using atrioventricular pacing, as atrial pressure was varied over a wide range by volume expansion. In paced hearts vagal stimulation depressed atrial contractile force but did not alter atrial receptor discharge when compared to paced hearts without vagal stimulation. These results indicate that the effect of vagal stimulation on atrial receptor discharge is an indirect one mediated through the rise in atrial pressure due to cardiac slowing rather than a direct effect on the atrial stretch receptor itself.