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There are a number of observations which suggest that acetylcholine exerts an excitatory influence over the medullary vasomotor center. Dhawan et al. (1) reported that both acetylcholine and carbachol produce a pressor response on intracerebroventricular (i.c.v.) administration in dogs and this pressor response is blocked by atropine. Sinha et al. (2) observed that hemicholinium, which blocks the synthesis of acetylcholine depresses the responsiveness of vasomotor center on i.c.v. administration as well as after topical application to the floor of the fourth ventricle. Release of acetylcholine by tyramine has been suggested to be involved in the pressor response produced by i.c.v. administration of tyramine (1). Pfeiffer et al. (3) studied several compounds to find out longer acting parasympathomimetic agents or precursors of acetylcholine which might affect the central nervous system. They reported parasympathomimetic and central effects of 2-dimethyl aminoethanol (deanol) and suggested that it owes the actions to its conversion to acetylcholine. We, therefore, thought it worthwhile to study the central vasomotor effects of deanol and to investigate if these effects are due to its conversion into acetylcholine.

A STUDY OF THE CENTRAL VASOMOTOR EFFECTS OF 2-DIMETHYL AMINOETHANOL (DEANOL)