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Sodium restriction affects sympathetic control mechanisms by blunting of the reflex pressor response to carotid sinus hypotension, which is reversible by section of vagal afferents. To obtain more direct evidence, sympathetic nerve activity was recorded from a renal nerve (RNA) in 16 normal (NS) and 13 sodium-depleted (SD) dogs anesthetized with morphine-pentobarbital. Integrated RNA was measured during changes in mean arterial pressure (MAP) produced by i.v. infusion of sodium nitroprusside (100 micrograms/kg/min) or phenylephrine (20 micrograms/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 less than 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.

Altered neural control of cardiovascular function in sodium-depleted dogs.