PERIPHERAL ACTION OF THE GANGLION BLOCKINC AGENTS

Abstract

It is generally accepted that the ganglion blocking agents such as tetraethylammonium or hexamethonium has scarcely any peripheral action, but tetraethylammonium exhibits a somewhat stronger acetylcholine-like action on the parasympathetic postganglionic effectors than hexamethonium (1). On the other hand, the vasopressor actions of intravenous adrenaline and some other sympathomimetic amines are greatly increased or prolonged after ganglionic transmission is blocked by these agents (2-4). The explanation on this phenomenon differs from each other. As the effects of these agents on some extirpated organs are almost negligible, Paton and Zaimis, and Moe, concluded that this phenomenon derived from the inactivation of the reflex compensatory haemodynamic mechanism. Page and Taylor considered that the phenomenon caused by tetraethylammonium a result of the release of noradrenaline-like substances from the liver. This potentiation occurs also after vagotomy or full atropinization. Therefore it can not result from the blockade of a parasympathetic reflex vasodilatation.
The experiments were directed to analyze further the adrenaline potentiation in other tissues and endeavoured to resolve whether the phenomenon is due to ganglionic. on postganglionic mechanism. The results revealed exactly that the ganglion blocking agents had a definite masked peripheral action beyond the action on the ganglion cells, which modified the response of the sympathetic postganglionic effectors to adrenaline, noradrenaline and the electrical postganglionic nerve stimulation.