Neurotransmission in the urinary bladder of rabbits and guinea pigs.

Abstract

Alpha, beta-Methyleneadenosine 5'-triphosphate (alpha, beta-mATP) produced transient contraction of strips of bladder taken from rabbits or guinea pigs, and mechanical responses to field stimulation at 5-100 Hz were reduced by this drug by 5-20%. Atropine reduced responses by approximately 50%, and both drugs together by 80-95%. In double sucrose gap experiments on the rabbit bladder, alpha, beta-mATP selectively reduced but did not abolish an initial excitatory junction potential (ejp), and atropine selectively abolished a late depolarization. In the guinea pig, a single ejp was partially inhibited by either alpha,beta-mATP or atropine. Residual responses were further reduced by tetrodotoxin in both species. The initial ejp and late depolarization in the rabbit were reduced in parallel by hemicholinium over 2 h, suggesting that release of acetylcholine (ACh) and the second transmitter by nerves may be coupled. ACh but not ATP produced an increase in intracellular concentration of inositol trisphosphate in dispersed smooth muscle cells from the rabbit bladder; ATP but not carbachol produced a small transient current across the cell membrane in this species. It is concluded that ACh mobilizes intracellular Ca2+ for contraction, whereas the effect of ATP is dependent on extracellular Ca2+.