MICTURITION AND PREMICTURITION CONTRACTIONS IN UNANESTHETIZED RATS WITH BLADDER OUTLET OBSTRUCTION

The cholinergic and purinergic neurotransmission involved in micturiti on contraction and premicturition contractile activity (bladder hypera ctivity) were investigated by continuous cystometry in unanesthetized rats with outlet obstruction. Adenosine triphosphate (ATP), administer ed intra-arterially close to the bladder, produced rapid, phasic dose- dependent increases in bladder pressure and micturition immediately af ter the injections. The percentage volume expelled was 74 +/- 9% after 5 mg./kg. Intra-arterial alpha,beta-methylene ATP also produced a rap id, phasic increase in bladder pressure and micturition immediately af ter the injection. The percentage volume expelled was 96 +/- 3% after 1 mg./kg.; the residual volume of the following voidings increased, an d the micturition pressure tended to decrease. However, dribbling inco ntinence was not produced. The amplitude of the premicturition contrac tions decreased significantly (p < 0.01) after the administration. Int raarterial carbachol produced rapid, longlasting dose-dependent increa ses in bladder pressure and micturition. The percentage volume expelle d was 88 +/- 4 after 5 mug./kg. Bladder capacity and micturition volum e decreased significantly (p < 0.05) during the following spontaneous voidings. Intra-arterial atropine (1 mg./kg.) increased bladder capaci ty (p < 0.01) and residual volume (p < 0.01), and tended to decrease m icturition pressure (by 25%) and micturition volume. However, micturit ion contractions still remained after the injection, even if they chan ged appearance, and were of shorter duration. Atropine had no effect o n the premicturition contractions. In the presence of atropine, alpha, beta-methylene ATP initially produced a rapid, phasic increase in blad der pressure with micturition. Then, dribbling incontinence was observ ed 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 tetro dotoxin (15 mug./kg.) inhibited micturition, and produced dribbling in continence in all animals tested (n = 6). However, the amplitude of th e premicturition contractions was not suppressed. Intra-arterial (+/-) -pinacidil (0.2 mg./kg.) significantly (p < 0.05) decreased both ampli tude and frequency of these contractions. It is concluded that both ch olinergic and purinergic transmission seem to be of importance for pre ssure generation and emptying of the bladder in rats with outlet obstr uction. The present results also give further support for the view tha t the premicturition contractions seen in these animals are of myogeni c origin.