Aortic nerve stimulation inhibits carotid baroreflex-induced bradycardia and systemic pressure decreases in dogs, suggesting central medullary interaction suppressing vagal efferents.
Subadditive baroreflex effects in dogs warrant no clinical translation; leaves open central interactions for human mechanistic studies.
In dogs anesthetized with morphine-chloralose, low-frequency high-intensity stimulation of the aortic nerve (AN) causes a modest reflex tachycardia and a rise in systemic pressure. Stimulation of the carotid sinus nerve or raising pressure in the isolated carotid sinus causes reflex bradycardia and a fall in systemic pressure. Combined stimulation of these reflexes resulted in less bradycardia and a smaller decrease in systemic pressure than the sum of the responses to separate stimulation (P less than 0.001). This suggests that the opposing reflexes interact in a manner whereby the carotid baroreflex responses are inhibited by the AN stimulation. This interaction occurs in the medullary centers and appears to involve primarily suppression of the vagal efferents to the heart. Baroreflex inhibition of sympathetic vasomotor activity also appears to be suppressed by AN stimulation. It is concluded that aortic cardiac sympathetic activity and in part by suppressing baroreflex-induced bradycardia.
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Pisarri et al. (1982) studied this question.
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