Introduction: Chronic baroreflex activation is a therapy for resistant hypertension and has potential as a therapy in heart failure.

We hypothesized that acute baroreflex activation therapy (CVRx, Inc.) would increase both the capacity of the abdominal venous circulation (lowering “preload”) and aortic conductance (reducing “afterload”).

Methods: Six 20-kg mongrel dogs were anaesthetized and ventilated. Arterial blood pressure (BP) and diaphragmatic aortic and caval flow (ultrasonic) were measured. Venous capacity changes were evaluated using a modified Brooksby-Donald technique^*. A CVRx electrode was affixed to the right carotid sinus.

BP and flow data were collected under control conditions and during device activation and drug infusions. Angiotensin II (ANG II) was infused to raise BP to hypertensive levels; the current from the device was then increased.

Results: Device activation decreased mean aortic BP 22.5±1.3 mmHg, decreased heart rate 14.7±3.4% and cardiac output 10.8±3.9%, increased aortic conductance 16.2±4.9%, and increased abdominal blood volume at a rate of 2.2±0.6 mL/kg/min (5-minute activations). ANG II infusion increased BP 40.3±3.4 mmHg and reduced venous capacitance at a rate of 1.1±0.5 mL/kg/min. Subsequent electrical stimulation restored BP to baseline while aortic conductance only returned to 82.3±3.3% of control. Venous capacitance increased at a rate of 3.4±0.7 mL/kg/min, reversing the ANG II effects.

Conclusions: Acute electrical activation of the carotid baroreflex increases arterial conductance, decreases BP, and increases venous capacitance. Modulation of venous capacitance may be an important effect of baroreceptor activation in hypertension and heart failure.