Neurogenic suppression of carotid sinus reflexes by vagal afferents in sodium-depleted dogs.

Reduction of sodium intake affects both the renin-angiotensin and sympathetic nervous systems, but the effects on the latter are less well understood. To clarify this relationship, the responsiveness of the baroreceptor reflex was compared in groups of normal and sodium-depleted dogs prepared with a single innervated carotid sinus and left vagus nerve after anesthesia with morphine-chloralose. Three weeks of sodium depletion did not affect the mean arterial blood pressure, but cardiac output (-50%) and stroke volume (-38%) were reduced, whereas there was a large compensatory increase in total peripheral resistance (115%). The pressor response to carotid occlusion in sodium-depleted dogs was significantly less (35 +/- 4 mmHg) than that obtained in normal dogs (61 +/- 5 mmHg). In the dogs treated with cholinergic blockade with atropine, this difference (-51%) persisted. In contrast, the pressor response to carotid occlusion in sodium-depleted dogs was significantly potentiated (112%) and restored in magnitude to that found in normal dogs after severing the only remaining vagus nerve. These data suggest that the cardiopulmonary and/or aortic vagal afferents are responsible for the blunting of baroreceptor reflexes during sodium depletion.