Abstract

The influence of gallamine, pancuronium, suxamethonium and d-tubocurarine on adrenergic neurotransmission was studied in the isolated saphenous vein of the dog. Pancuronium but not the other muscle relaxants increased significantly the response to sympathetic stimulation and to exogenous norepipephrine; these increases were abolished after blockade of neuronal uptake by cocaine. Pancuronium and gallamine inhibited both the relaxation produced by lower doses of acetylcholine added during sympathetic stimulation (prejunctional effect) and the direct contractions evoked by high doses of the amine (postjunctional effect). In strips previously incubated with [3H]norepinephrine, gallamine had no effect on [3H]norepinephrine efflux in basal conditions and during sympathetic stimulation; it increased markedly the efflux evoked by sympathetic stimulation in the presence of acetylcholine confirming that gallamine inhibits the prejunctional effect of the latter on adrenergic transmission. When extrapolated to the intact organism, the present experiments indicate that gallamine and pancuronium augment the release of norepinephrine in vascular tissue under vagal control, which explains in part the cardiovascular effects of these muscle relaxants.