PHARMACOLOGICAL STUDIES ON SUPERSENSITIZATION. XI. INHIBITORY EFFECT OF DIBENAMINE ON TRIPELENNAMINE-N, N-DIMETHYL-N', N'-DIBENZYLETHYLENEDIAMINE- AND N, N'-DIBENZYL-N', N'-DIMETHYL-1, 2-PROPANEDIAMINE-INDUCED SUPERSENSITIVITY OF ISOLATED VAS DEFERENS OF GUINEA PIG

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Effects of dibenamine on tripelennamine-, N, N-dimethyl-N', N'-dibenzylethylenediamine (DBED)- and N, N-dibenzyl-N', N'-dimethyl-1, 2-propanediamine (DBPD)-induced supersensitivity of isolated vas deferens of guinea pig were examined. Dibenamine attenuated the degree of tripelennamine- and DBED-induced increase in sensitivity to acetylcholine and potassium in standard Tyrode solution, but did not affect the degree of DBPD-induced increase in sensitivity to acetylcholine. Dibenamine diminished the degree of tripelennamine-induced increase, but did not affect the degree of DBED-induced increase, in maximum response to Ca²⁺ of partially depolarized vas deferens. Dibenamine diminished the degree of tripelennamine- and DBED-induced augmentation of potassium-contraction in Ca²⁺-free Tyrode solution, but did not affect that of acetylcholine-contraction. These results suggest that dibenamine prevent tripelennamine- and DBED-induced increase in Ca²⁺-influx (including extracellular Ca²⁺-superficial Ca²⁺ exchange) induced by acetylcholine and potassium. It is also suggested that DBPD potentiates acetylcholine-contraction by dibenamine-insensitive mechanisms.