Abstract
There is adaptation of the cardiac vagal efferent responses to stimulation of the arterial baroreceptors by a series of brief intracarotid pressure pulses, by a sustained elevation of pulsatile systemic pressure, or by sustained steady increases in intracarotid pressure. This was demonstrated here in experiments on anesthetized dogs. Trains of brief intracarotid pressure pulses were delivered to carotid baroreceptors at varying interstimulus intervals. Reflex bradycardia was evoked by the first stimulus of a train but as succeeding stimuli were placed closer to those preceding them, they became less effective in evoking reflex bradycardia. This attenuation of the heart rate response was not due to attenuation of the responses of baroreceptor nerve endings to repeated brief stimuli, or to reflex changes in systemic blood pressure. Activity in single cardiac vagal efferent fibers was recorded in response to pairs of intracarotid pressure pulses, to step changes in non-pulsatile carotid blood pressure and to changes in pulsatile systemic blood pressure. Adaptation of cardiac vagal discharge over a period of 10 s or more, to both pulsatile and non-pulsatile and non-pulsatile increases in blood pressure, was shown. The slow time course of the adaptation of vagal discharge makes it most unlikely that it can be completely accounted for by adaptation of the baroreceptor nerve endings themselves. Adaptation apparently occurs centrally, along the baroreceptor to vagal pathway.