The motor activity of the rat bladder elicited by transmural electrical stimulation was abolished in the presence of 200 nM tetrodotoxin but not of 1 microM atropine plus 3.4 microM guanethidine. Tissue preincubation with 20 microM, alpha, beta-methylene ATP reduced but did not obliterate the electrically-induced motor effect. Bradykinin (BK) caused a short-lasting motor response while it potentiated, in a concentration-dependent fashion, the 0.15-5 Hz-induced muscle twitching. The facilitatory action of the peptide lasted for at least 5 min and was blocked by the BK-B2 receptor antagonist D-Arg0 [Hyp3, Thi5,8, D-Phe7]-BK. The motor response caused by the exogenous application of adenosine 5'-triphosphate (ATP) was almost immediate and lasted less than 30 s; it was also potentiated by BK-B2 receptor activation, an effect that was reduced in a concentration-dependent manner by pretreatment with the BK-receptor antagonist.