Abstract

When barbiturate-anesthetized dogs were given pronethalol or guanethidine, ST 155 [2-(2,6-dichiorophenylamino)-2-imidazoline HCI] caused bradycardia and induced bradycardic responses to epinephrine and norepinephrine. The catecholamines and ST 155 initially did not affect heart rate of pronethalol-pretreated dogs, but, with repeated small doses of ST 155, gradually increasing bradycardias were obtained without comparable changes in the pressor effects of these agents. Despite complications introduced by changes in sympathetic tone, the influence of repeated doses of ST 155 was also recognizable in dogs without pronethalol pretreatment. Pronethalol, interruption of pressure-sensitive reflex pathways or the reduction of pressor responses by alpha adrenergic blockade separately modified the size and duration of the bradycardia and in combination abolished the bradycardia of ST 155. In morphine-chloralose-anesthetized dogs, in which heart rate appeared to be largely under vagal control, ST 155 caused bradycardia which was not affected by sympathetic blockade but was abolished by atropine or bilateral vagotomy. These results indicate that, in addition to the reported central suppression of sympathetic outflow, ST 155 can cause bradycardia by enhancing pressuresensitive, compensatory reflexes.