Bradykinin facilitates the purinergic motor component of the rat bladder neurotransmission.

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.