Anticholinergics have been suggested to reduce the nocturnal urine volume (Yokoyama 2013). In basic research to verify that study's findings, Watanabe (2013) confirmed that the anticholinergics, imidafenacin (IM) and, tolterodine (TO) administered separately to a rat diuretic model reduced the urine volume, but no effects of these anticholinergics were observed in rats in which bladder sensory C fibers were desensitized with resiniferatoxin.  It was also reported that the rat urinary bladder absorbs water and salts under the full-filled condition (Morizawa 2018), and the following animal experiments were thus conducted to investigate the following mechanisms that may underlie the reduction of urine output with anticholinergics; (1) the reabsorption of urine in the bladder, and (2) the reabsorption of urine in the kidneys.

Exp. 1: Under urethane anesthesia, both ureters of 6- to 8-week-old female SD rats were ligated, and a catheter was placed in the bladder transurethrally. While the bladder pressure was being measured, 0.3% saline, 0.9% saline, 5% glucose solution, 10% glucose solution, or soy bean oil were injected (n=6 rats each) until the bladder pressure reached 30 cmH2O. One minute later, vehicle (VE), IM, atropine (AT), or TO was intravenously administered, and the amount of solution in the bladder was measured 2 hr later. The osmotic pressure, specific gravity, and electrolyte concentration of the solution were measured.
Exp. 2: Bilateral ureters of other similar rats were cannulated with a small-dia. catheter (SP-10 catheter, inside diameter: 0.28mm, outside diameter: 0.61mm, NATSUME SEISAKUSHO CO., LTD. (tokyo, Japan)), and physiological saline was continuously administered intravenously to obtain a diuretic state under urethane anesthesia. Two hours later, anticholinergics (VE, IM, AT, TO) were intravenously administered. The amount of urine was measured every hour. The same experiments were performed in rats with C fibers desensitized with resiniferatoxin.

Physiological saline injected into the bladder was absorbed from the bladder, and the absorption rate was approx. 10% of the injected amount. This absorption rate was constant even when the anticholinergic drugs or other drugs were administered (Fig. 1). 
The absorption rates of the 10% glucose solution and the soy bean oil were significantly low. There was no change due to C -fiber desensitization. Electrolyte absorption was also observed with water. The rats' renal urine volume peaked 3 hr after the intravenous administration of the saline. IM significantly suppressed the urine production in a dose-dependent manner (p≺ 0.01 vs. vehicle; Fig. 2). The peak of urine production was also suppressed by the AT and TO administrations, even when the C -fibers were desensitized.

These results suggest that urine production may be suppressed by anticholinergics via an increase in the reabsorption of urine in the kidneys.

The urinary absorption mechanism through the bladder epithelium was not activated by the present administration of antichlinergics. These results suggest that urine production may be suppressed by anticholinergics via an increase in the reabsorption of urine in the kidneys. This action was not dependent on afferent C fibers.