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The effects of debrisoquin and bretylium on adrenergic nerves as revealed by fluorescence histochemistry.

The effects of debrisoquin (0.1-100 mg/kg), bretylium (0.1-50 mg/kg) and nialamide (5-100 mg/kg) on the uptake, storage, metabolism and release of norepinephrine (NE) in adrenergic neurons were studied by the fluorescence histochemical method of Falck and Hillarp in the iris of the albino rat. These agents, given 1 to 16 hours before NE (0.1 mg/kg i.v.) to reserpine-treated (10 mg/kg i.p.) rats, permitted the accumulation of this catecholamine in the adrenergic nerves. Pretreatment with these drugs prevented reserpine (2.5 mg/kg i.p.)-induced NE depletion. These effects of debrisoquin and bretylium were more transient than those of nialamide and, contrary to the latter, were reduced by pretreatment with desmethylimipramine or protryptaline. However, the former agents were 10 times more potent than nialamide. Large doses of debrisoquin or bretylium blocked nerve transmission and the NE-depleting effects of reserpine and H 44/68, an inhibitor of NE biosynthesis in combination with nerve stimulation; smaller doses reduced the depleting effects without altering nerve transmission. Debrisoquin, bretyliurn and desmethylimipramine, but not nialamide, reduced the uptake of α-methyl-NE, a poor monoamine oxidase substrate, by the iris of reserpine-treated rats. Finally, debrisoquin (50 mg/kg i.p.) was shown to increase the content of H 3 -NE by the hearts of reserpine-treated (10 mg/kg i.p.) rats. The data suggest that debrisoquin and bretylium are reversible intraneuronal monoamine oxidase inhibitors whose potency in adrenergic neurons occurs because of accumulation by membrane transport. The monoamine oxidase-inhibiting and neuron-blocking activities were separable.