Demonstration that the atria, ventricles, and lungs each are responsible for a tonic inhibition of the vasomotor center in the dog

To localize the areas of the cardiopulmonary region involved in tonic inhibition of the vasomotor center, anesthetized dogs were subjected to sinoaortic denervation and diaphragmatic vagotomy. Afferent vagal nerve traffic was interrupted in the neck by cooling. With the venous return taken from the venae cavae, oxygenated extracorporeally, and returned to the aorta, the heart was removed, leaving the ventilated lungs (condition 1), and the lungs and the ventricles were removed, leaving the beating atria (condition 3). With the venous return taken from the pulmonary arteries, oxygenated extracorporeally, and returned to the left atrium, the lungs were removed, leaving the intact working heart (condition 2), and the lungs were removed and the atria were denervated, leaving the working innervated ventricles (condition 4). Vagal cooling increased aortic pressure by 25 ± 2 (SE) mm Hg in condition 1, by 36 ± 2 mm Hg in condition 2, by 29 ± 2 mm Hg in condition 3, and by 29 ± 7 mm Hg in condition 4. Removing the atria in condition 3 or devervating the ventricles in condition 4 abolished the reflex response. Thus, afferent vagal nerves from the lungs and the heart tonically inhibit the vasomotor center. The inhibition exerted by the heart is caused by receptors in the atria and the ventricles.