Micturition and premicturition contractions in unanesthetized rats with bladder outlet obstruction.

The cholinergic and purinergic neurotransmission involved in micturition contraction and premicturition contractile activity (bladder hyperactivity) were investigated by continuous cystometry in unanesthetized rats with outlet obstruction. Adenosine triphosphate (ATP), administered intra-arterially close to the bladder, produced rapid, phasic dose-dependent increases in bladder pressure and micturition immediately after the injections. The percentage volume expelled was 74 +/- 9% after 5 mg/kg. Intra-arterial alpha,beta-methylene ATP also produced a rapid, phasic increase in bladder pressure and micturition immediately after the injection. The percentage volume expelled was 96 +/- 3% after 1 mg./kg; the residual volume of the following voidings increased, and the micturition pressure tended to decrease. However, dribbling incontinence was not produced. The amplitude of the premicturition contractions decreased significantly (p < 0.01) after the administration. Intra-arterial carbachol produced rapid, longlasting dose-dependent increases in bladder pressure and micturition. The percentage volume expelled was 88 +/- 4 after 5 micrograms./kg. Bladder capacity and micturition volume decreased significantly (p < 0.05) during the following spontaneous voidings. Intra-arterial atropine (1 mg./kg.) increased bladder capacity (p < 0.01) and residual volume (p < 0.01), and tended to decrease micturition pressure (by 25%) and micturition volume. However, micturition contractions still remained after the injection, even if they changed appearance, and were of shorter duration. Atropine had no effect on the premicturition contractions. In the presence of atropine, alpha,beta-methylene ATP initially produced a rapid, phasic increase in bladder pressure with micturition. Then, dribbling incontinence was observed in 1 of 5 animals. Hexamethonium, administered intra-arterially in doses producing urinary retention and dribbling incontinence (20 or 40 mg./kg.), increased the amplitude of the premicturition contractions, but decreased the frequency of the contractions. Intra-arterial tetrodotoxin (15 micrograms./kg.) inhibited micturition, and produced dribbling incontinence in all animals tested (n = 6). However, the amplitude of the premicturition contractions was not suppressed. Intra-arterial (+/-)-pinacidil (0.2 mg./kg.) significantly (p < 0.05) decreased both amplitude and frequency of these contractions. It is concluded that both cholinergic and purinergic transmission seem to be of importance for pressure generation and emptying of the bladder in rats with outlet obstruction. The present results also give further support for the view that the premicturition contractions seen in these animals are of myogenic origin.