The decrease in neurogenic bladder contraction possibly accompanied by the decreased density of muscarinic receptors, the potentiation of neurogenic bladder contraction with 5-hydroxytryptamine probably due to facilitated cholinergic transmission and the enhanced contractility to 5-hydroxytryptamine would be at least in part involved in bladder dysfunction associated with hyperglycemia.

pretreatment with intraperitoneal injection of CYP (150 mg/kg) 24 h before cystometry. In control rats during intravesical saline, the effects of above drugs on the bladder activity were also examined. RESULTSThe intercontraction intervals (ICI) in AAand CYP-treated rats were significantly shorter than those in control rats. Neostigmine (i.t.) significantly increased ICI dose-dependently without changing maximum voiding pressure in all groups. The mean ( SEM ) maximal percentage increases in ICI after i.t. neostigmine as compared with the pretreatment value in control, AA-and CYP-treated rats were 93.2 (18.5)%, 117.5 (20.2)% and 200.7 (19.6)%, respectively. The percentage increases of ICI in the CYP-treated group were significantly ( P < 0.05) higher than those in the AAtreated or control groups. In all groups, pretreatment with atropine, but not MEC, almost completely antagonized the inhibitory effects of neostigmine. OXO-M produced almost the same effects as that of neostigmine in all groups. Conversely, i.t. epibatidine decreased the ICI in all groups and these excitatory effects were completely antagonized by pretreatment with MEC and significantly inhibited by pretreatment with MK-801(noncompetitive N -methyl-Daspartate receptor antagonist). CONCLUSIONSThese results indicate that accumulation of ACh by AChE inhibition in the spinal cord can ameliorate frequent urination in chemical cystitis via mAChRs, but not nAChRs.