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.

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.