Electrical stimulation of the carotid baroreceptor has been shown to be an effective therapy for patients with (resistant) hypertension. However, the exact mechanism leading to blood pressure reduction is not fully elucidated. We measured left ventricular pressure and volume, ascending and abdominal aortic pressure using high-fidelity transducers in 9 anaesthetized dogs (24.8 ± 2.9 kg) at baseline and during electrical stimulation of the carotid baroreceptors. Therapy significantly (all P<0.001) lowered mean (from 81.1±7.6 to 54.8±5.5 mmHg), systolic (from 95.7±7.8 to 78.6±6.0 mmHg) and diastolic (from 66.6±8.3 to 41.4±6.2 mmHg) pressures. Cardiac output remained unchanged, but stroke volume tended to increase while heart rate decreased (83.5±15.3 to 67.2±19.3 beats/min, P=0.002). Systemic vascular resistance decreased from 1.25±0.50 to 0.92±0.44 AU, P=0.002). There was no change in central-to abdominal pulse transit time, and we could not unequivocally demonstrate a change in total arterial compliance. Therapy had a drastic effect on the morphology of the pressure waveforms and on the relationship between abdominal and central aortic pressure. Pressure was amplified at baseline but damping of the pressure pulse along the aorta was observed during stimulation, suggesting a drastic impact of therapy on pressure wave reflection. This was confirmed by a decrease in the magnitude of wave reflection (from 0.54±0.13 to 0.39±0.08, P=0.014). We conclude that, in an acute animal model, carotid baroreceptor stimulation significantly lowers blood pressure through vasodilation, with important effects on patterns of wave reflection. Further research is mandatory in experimental (conscious) models of hypertension and in patients.