Excitatory Nerve Conduction Changed In a Partial BOO-induced OAB Rat Model

Abstract

Abstract Background Overactive bladder (OAB) is a common, long-term symptom complex with a high prevalence in women worldwide. The pathogenesis of OAB has not been elucidated. This study investigated the excitatory purinergic and cholinergic nerve conduction in OAB rat model induced by partial bladder outlet obstruction(PBOO）. Methods Model rats underwent bladder outlet obstruction surgery. In the 2nd, 3rd, and 4th week after surgery, metabolic cages were used to detect the 12-hours Urine volume of the rats in the sham and model groups. The urodynamic parameters Bladder leak point pressure (BPLL), Maximum voiding pressure (MVP), Residual volume (RV), Maximum bladder capacity (MBC), Bladder compliance (BC), Voided efficiency (VE), and Non-voiding contractions (NVCs) were also detected. Besides, the time point above examined the contractile responses of isolated detrusor muscles to electrical and carbachol stimulation. 4th week after surgery, the bladders of both groups were taken for hematoxylin, eosin (H&E), and Masson’s trichrome staining. Besides, real-time qPCR and Western blot were performed to quantify the expression of Choline acetyltransferase(ChAT) and Solute carrier family 17 member 9 (SLC17A9). Results At week 4, compared with the sham group, the 12 h Urine volume increase significantly. The BLPP、MVP、VE、MBC、NVCs increased significantly, and the VE was significantly reduced. The contractile responses of isolated detrusor muscles to electrical and carbachol stimulation were significantly increased. In 4 week PBOO group, the bladder wall and the ratio of bladder muscle to collagen within the bladder smooth muscle layer wall were significantly higher than in the sham group. ChAT and SLC17A9 mRNA and protein expression in OAB model rats was significantly increased. Conclusions 4 weeks after PBOO, the OAB model was successfully established. The gene and protein expressions of ChAT and SLC17A9 were increased in the bladder of OAB model, suggesting that OAB may relate to the increased excitatory purinergic and cholinergic nerve conduction.