Nonalgebraic interaction between pressor and depressor reflexes in dogs: evidence for a central site of action

In a previous study (Kendrick, JE and Matson, G 1979, Amer J Physiol 327:H662-H667) we demonstrated that the vascular responses in dogs to electrical stimulation of aortic nerve (AN) pressor and carotid sinus nerve (CSN) depressor afferents did not sum algebraically. We suggest this results from a reflex interaction which occurs in the central nervous system. The present study extends earlier studies by recording sympathetic vasomotor in chloralose-anesthetized dogs. Stimulation of the CSN reduced sympathetic activity by 51 +/- 20 (SD)%. AN stimulation (2 Hz) caused a 17 +/- 12% increase in sympathetic activity. Combined stimulation of the ipsilateral CSN and AN caused 0 +/- 28% change rather than a 34% decrease expected by an additive interaction. The interaction recorded in this study from the sympathetic outflow is therefore consistent with the previously reported vascular responses (cited above) and implicates central nervous site(s) of action. A conditioning stimulus train to CSN inhibited sympathetic discharges to AN test stimuli. This inhibition was prevented by pairing an AN stimulus with the CSN stimulus train. The AN pressor reflexes act in part by increasing sympathetic activity and in part by suppressing the baroreflexes.