Neural mechanisms involved in acetylstrophanthidin-induced bradycardia.

The role of neural sites in the bradycardia produced by acetylstrophanthidin (14.1, 22.5 and 35.5 mug/kg) was studied in chloralose-anesthetized cats with efferent vagal tone blocked by atropine. The sites were: carotid sinus baroreceptors, aortic arch baroreceptors, cardiac sensory receptors, nodose ganglion receptors and central nervous system structures. The role of each site was determined by selective ablation of all sites except the one under study. Significant slowing in heart rate occurred when: 1) only carotid sinus baroreceptors were intact; 2) only aortic arch baroreceptors were intact and 3) only cardiac sensory receptors were intact. No cardiac slowing was observed when only nodose ganglion receptors, central sympathoinhibitory sites and beta adrenergic receptors were intact. These results indicate that in atropine-treated cats, the further slowing in heart rate produced by acetylstrophanthidin arises from activation of reflex sites located in the carotid sinus, aortic arch and myocardium.