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Aims: The aim of this study is to investigate whether ketamine could relieve the social stress (SS)‐related bladder dysfunction in mice. Materials and Methods: The FVB mice were randomly assigned to either undergo SS exposure for 60 minutes per day on seven consecutive days for 4 weeks (SS1) or control without SS (SS0). The SS0 were then allocated to single or no injection of ketamine (SS0K1 and SS0K0). In the group of SS1, the SS1 mice were allocated to receive single injection of saline (SS1K0), single dose (SS1K1) or five daily dose of (SS1K5) ketamine injection (25 mg/kg/day/ip) since day 22. In vivo cystometry and tissue bath wire myography were performed on day 29. Serum and urine level of brain‐derived neurotrophic factor (BDNF) were measured with enzyme‐linked immunosorbent assay. Results: In mice without social stress exposure, ketamine administration did not significantly affect voiding frequency (P >.05). SS1K0, SS1K1, and SS1K5 had significantly lower voiding frequency than that of control (SS1K0) (each n = 15, P <.05). Ketamine administration reversed the trend of decreased voiding frequency in SS1 mice. Stressed mice had significant higher serum level of BDNF that reduced by short‐term ketamine. Stressed mice had detrusor overactivity and impaired detrusor contractility which were not reversed by short‐term ketamine. Conclusions: Social stress leads to elevated serum BDNF, infrequent voiding, detrusor overactivity, and impaired contractility. Short‐term administration of ketamine may improve SS‐related infrequent voiding and elevated serum BDNF level. However, ketamine did not improve SS‐related bladder dysfunction on urodynamic and myography studies. [ABSTRACT FROM AUTHOR]

Objective: We have demonstrated that phenylephrine (PE) activates the capsaicin-sensitive nerves, and then activates capsaicin-sensitive nerves to release an unknown substance that facilitates the release of norepinephrine (NE) from adrenergic nerves. Subsequently, NE stimulates β-ARs in the detrusor muscle in mice, leading to neurogenic relaxation of the urinary bladder (UB). Materials and Methods: We examined if there existed sensory-motor dysfunction in UB of aging mice. To investigate the change of PE-induced detrusor relaxation in aging male-C57BL/6 mice (12- vs. 24-month-old mice), UB strips from mice were isolated, cut into strips, and mounted in the organ bath. Results: The UB strip contractility responding to various agents was estimated using tissue bath wire myography. Acetylcholine (ACh) and KCl-induced UB strips contraction was not significantly different between 24- and 12-month mice. NE-induced UB strips relaxation was significantly lower in 24-month than 12-month mice. Denuded bladder strips showed similar decreased relaxation response to NE. This NE-induced relaxation was inhibited by silodosin and lidocaine. PE did not induce contraction in UB strips of aging mice. In contrast, PE-induced relaxation was weaker in 24-month than 12-month mice. Conclusion: Our results suggested that the PE-induced relaxation was age related. Aging seemed to lead the sensory-motor dysfunction. More animal and human studies are required to prove this concept and its clinical usefulness in the future. [ABSTRACT FROM AUTHOR]