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1 Department of Pharmacology, College of Medicine, University of Iowa, Iowa City, Iowa
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'-Bis-(dimethylammonium-acetaldehyde diethylacetal)-p,p'-diacetylbiphenyl bromide (DMAE) has been found to potentiate responses to sympathetic nerve stimulation and catecholamine administration. Potentiation of the contraction of the cat nictitating membrane after cervical sympathetic nerve stimulation was more pronounced at low than at high frequency. The height and duration of the contractions of the nictitating membrane in response to epinephrine or norepinephrine and the pre- or postganglionic stimulations of the cervical sympathetic nerve were increased markedly after DMAE. The blood pressure in cats and dogs was increased after administration of DMAE. In reserpine-pretreated dogs and approximately 10% of the nonreserpine-pretreated dogs, a depressor response to DMAE was observed. Blood pressure responses to epinephrine and norepinephrine in the normal and reserpine-pretreated cats and dogs were increased significantly after DMAE. Cocaine and DMAE appeared to demonstrate parallel ability to enhance sympathomimetic effects of various phenylethylamine derivatives with direct actions. DMAE and cocaine did not potentiate responses to sympathomimetic amines with indirect actions. Tyramine responses in the isolated guinea-pig atria were antagonized by DMAE. Similarities and differences between DMAE and cocaine are discussed. DMAE is a close structural analog of hemicholinium but demonstrates marked differences in pharmacologic properties.