SUMMARY Sodium restriction affects sympathetic control mechanisms by blunting of the reflex pressor response to carotid sinus hypotension, which is rerersible by section of vagal afferents. To obtain more direct evidence, sympathetic nerre activity was recorded from a renal nerve (RNA) in 16 normal (NS) and 13 sodiumdepleted (SD) dogs anesthetized with morphine-pentobarbital. Integrated RNA was measured during changes in mean arterial pressure (MAP) produced by i.v. infusion of sodium nltroprusslde (100 Mg/kg/min) or phenylephrine (20 Mg/kg/min). The classical inverse relationship between MAP and integrated RNA was found before and after bilateral vagotomy (VAGT) in both NS and SD dogs. However, RNA in SD dogs, expressed as % of maximal neural firing, was significantly less at any blood pressure level when compared to NS dogs. In addition, the critical pressure (point at which RNA ceased) was reduced in SD vs NS dogs (p < 0.002). The decreased sympathetic neural firing in SD dogs was abolished after bilateral VAGT, confirming the pronounced buffering effects of vagal afferents on RNA in salt-depleted dogs. C HRONIC sodium depletion (SD) may produce significant alterations in autonomic nervous system function that do not conform to the usual understanding of the effect of increased blood levels of angiotensin II (All) upon neurogenic drive.1 Although All certainly acts to augment sympathetic efferent activity, in the dog the state of the sodium balance appears to modify significantly, and in an unexpected manner, the expression of the interplay between the renal pressor and the sympathetic nervous systems.A series of correlated studies involving investigation of baroreceptor reflexes, 1 -• cardiac function, 4 and measurements of catecholamines in both plasma and cerebrospinal fluid* support this conclusion. The studies were prompted when the carotid occlusion (CO) reflex was found to be sharply inhibited in dogs subjected to SD of 3 weeks' duration. 1 -* Suppression of the characteristic rises in heart rate and cardiac output persisted even after cholinergic blockade with atropine." However, section of the cervical vagus nerves markedly potentiated the CO reflex to the levels found in normal vagotomized animals..The augmented pressor response was now accompanied by prominent increases in stroke volume and cardiac out- put.' These data suggested that, in the SD state, removal of the inhibitory activity from the carotid sinus barorcceptors during CO was not sufficient to liberate the vasomotor centers from the additional input of vagal afferents probably discharging at rates above their tonic normal influence.The objective of the present study was to determine whether this peculiar effect of SD upon cardiovascular reflexes could be documented more directly by electroneurographic recordings of sympathetic nerve activity both before and after section of the vagus nerves.
MethodsExperiments were performed in 29 male mongrel dogs weighing between 17 and 23 kg. Thirteen animals were fed a sodium-restricted diet containi...