Abstract

In dogs anesthetized with morphine-chloralose, strong, low-frequency (2 Hz) electrical stimulation of the aortic nerve (AN) causes pressure in the perfused hindlimbs to rise. This pressor response is followed by a large depressor phase upon cessation of stimulation. Simultaneous stimulation of the ipsilateral carotid sinus nerve (CSN) with intermittent trains of stimuli enhanced the AN pressor response by 113%. Similar stimulation of the contralateral CSN had little effect on the AN pressor response. Constant-frequency stimulation of the ipsilateral CSN also failed to enhance this response. Possible mechanisms of the interaction between these antagonistic reflexes were investigated. The results suggest that the augmentation of the AN pressor response results from a central neuronal interaction between these antagonistic reflexes.

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