POTENTIATION BY [4,4'-BIPHENYLENEBIS(2-OXOETHYLENE)]BIS[(2,2-DIETHOXYETHYL) DIMETHYLAMMONIUM BROMIDE] (DMAE) OF THE SYMPATHETIC COMPONENT OF THE VASOPRESSOR RESPONSE TO ANGIOTENSIN

¹ Department of Pharmacology, College of Medicine, University of Iowa, Iowa City, Iowa

[4,4'-Biphenylenebis(2-oxoethylene)]bis[(2,2-diethoxyethyl)dimethylammonium bromide] (DMAE) and cocaine HCl were evaluated for their ability to alter the pressor response to 0.2 to 1.0 µg/kg of angiotensin II amide (A), 0.2 to 1.0 µg/kg of norepinephrine bitartrate (NE) and 50 and 100 µg/kg of tyramine hydrochloride. DMAE (0.9-2.7 mg/kg) potentiated significantly the pressor response to A and to NE in dogs. DMAE did not affect the pressor response to tyramine. Cocaine (0.8-5.0 mg/kg) potentiated the duration, but not the intensity, of the pressor response to A. Cocaine potentiated the pressor response to NE and blocked the effect of tyramine on blood pressure. Pyrogallol (40 mg/kg) and hexamethonium bromide (15 mg/kg) did not affect DMAE-induced potentiation of the pressor response to A and NE. Guanethidine monosulfate (15 mg/kg), bretylium tosylate (15 mg/kg), phentolamine hydrochloride (2 mg/kg) and reserpine (0.25 mg/kg) blocked DMAE-induced potentiation of the pressor response to A. In vitro in the isolated, perfused mesenteric arteries of the dog, the effects of these drugs on DMAE-induced potentiation of the responses to A and NE paralleled those results observed in vivo. It is suggested that DMAE does not block the reuptake of neurotransmitter at the nerve terminals of adrenergic nerves but instead facilitates the ability of A to release NE.