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The effect of 4,4'-biphenylenebis-((2-oxoethylene)-bis-(2,2-diethoxyethyl))dimethylammonium dibromide (DMAE) on the responses of tissues innervated by short adrenergic neurons to catecholamines and ionic stimulants.

The effect of DMAE on contractile responses of tissues innervated by short adrenergic neurons to norepinephrine, tyramine, KC1, BaCl3, CaCI2 and transmural stimulation was evaluated with the superfused rat vas deferens and guinea-pig seminal vesicle preparations. DMAE enhanced the responses of these tissues to tyramine, BaCl3, and transmural stimulation in concentrations (1-10 µg/ml) which did not affect the responses to norepinephrine, KCl or CaCl3,. When CaCl3 was omitted from the superfusate, DMAE enhanced the responses of the vas deferens to CaCl3 and BaCl3. Nerve terminal blockade with bretylium or guanethidine and depletion of neurotranemitter with reserpine abolished DMAE-induced potentiation of the responses of these tissues to BaCl and CaCl3. These results demonstrate that the effects of DMAE appear to be localized at the postganglionic nerve terminal membrane. The results also suggest that DMAE may alter neuronal permeability to divalent cations involved with the release of neurotransmitter.