Epidemiological studies link habitual snoring and stroke, but mechanisms involved are poorly understood. One previously advanced hypothesis is that transmitted snoring vibration energy may promote carotid atheromatous plaque formation or rupture. To test whether vibration energy is present in carotid artery walls during snoring we developed an animal model in which we examined induced snoring (IS)-associated tissue energy levels. In six male, supine, anesthetized, spontaneously breathing New Zealand White rabbits, we surgically inserted pressure transducer-tipped catheters (Millar) to monitor tissue pressure at the carotid artery bifurcation (PCT) and within the carotid sinus lumen (PCS; artery ligated). Snoring was induced via external compression (sandbag) over the pharyngeal region. Data were analyzed using power spectral analysis for frequency bands above and below 50 Hz. For frequencies below 50 Hz, PCT energy was 2.2 (1.1–12.3) cmH₂O² [median (interquartile range)] during tidal breathing (TB) increasing to 39.0 (2.5–95.0) cmH₂O² during IS (P = 0.05, Wilcoxon's signed-rank test). For frequencies >50 Hz, PCT energy increased from 9.2 (8.3–10.4) x 10⁻⁴ cmH₂O² during TB to 172.0 (118.0–569.0) x 10⁻⁴ cmH₂O² during IS (P = 0.03). Concurrently, PCS energy was 13.4 (8.5–18.0) x 10⁻⁴ cmH₂O² during TB and 151.0 (78.2–278.8) x 10⁻⁴ cmH₂O² during IS (P < 0.03). The PCS energy was greater than PCT energy for the 100–275 Hz bandwidth. In conclusion, during IS there is increased energy around and within the carotid artery, including lower frequency amplification for PCS. These findings may have implications for carotid atherogenesis and/or plaque rupture.