Pharmacological alterations of vagally induced tachycardia in anesthetized dogs

Abstract

Frequency-dependent tachycardia was obtained during vagal stimulation in anesnthetized, atropine-treated (1 mg/kg, i.v.) dogs. Vagally induced tachycardia was enhanced in both magnitude and duration by desipramine, whereas the magntide of tachycardia in response to cardioaccelerator nerve stimulation was not markedly enhanced. Vagal tachycardia was not inhibited by guanethidine (1 mg/kg, i.v.) but was markedly reduced after ganglion blockade by chlorisondamine (2 mg/kg, i.v.) or hexamethionium (10 mg/kg, i.v.). β-Receptor blockade by 1-oxprenolol (0.25 mg/kg, i.v.) totally blockade the response. Reserpine pretreatment decreased cardiac responses to sympathetic nerve stimulation to a greater degree than to vagal stimulation. From these results, it is suggested that the vagally induced tachycardia may be explained by acetylcholine (Ach)-mediated release of catecholamine from stores other than those susceptible to sympathetic nerve stimulation and these stores may reside in chromaffin tissue.