Locus of the adrenergic blocking action of Dibenamine

The recent demonstration of the high potency and specificity of the adrenergic blocking action of N, N-dibenzyl--chloroethyl amine (Dibenamine) (1, 2) raises the question of its locus and mode of action. Data presented previously (2) have ruled out any major effect on autonomic ganglia or postganglionic neurones or on the release, alteration or destruction of epinephrine and sympa-thin. Figure 1 illustrates most of these points. Here the nicotinic reaction to carbachol in an atropinized cat treated with Dibenamine illustrates the normal reactivity of the sympathetic ganglia and adrenal medulla. Although the pressor ’ effect of the sympatho-adrenal discharge is reversed by Dibenamine, the vascular response persists for almost exactly the same period of time as before, indicating a comparable course of release and destruction of epinephrine and sympathin. The same conclusion is suggested by the fact that Diben-amine does not markedly alter the sinus tachycardia induced by epinephrine (3) or circulating sympathin. In vitro experiments were also reported as evidence for the absence of any direct interaction between epinephrine and Dibenamine