Faculty of Health Sciences and Medicine, Centre for Urology Research, Bond University, Gold Coast, Australia.
PLoS One. 2022 Apr 21;17(4):e0266458. doi: 10.1371/journal.pone.0266458. eCollection 2022.
Psychological stress causes bladder dysfunction in humans and in rodent models, with increased urinary frequency and altered contractile responses evident following repeated environmental stress exposure. However, whether these changes persist after removal of the stressor is unknown, and the aim of this study was to determine if stress-induced changes in voiding behaviour and bladder function recover following removal of the stressor. Adult female mice were allocated to three groups: Unstressed, Stressed or Stressed + Recovery. Animals in the stressed groups were exposed to water avoidance stress for 1h/day for 10-days, with unstressed animals age-matched and housed under normal conditions. For recovery studies, animals were housed without stress exposure for an additional 10-days. Voiding behaviour was assessed periodically and animals sacrificed on day 10 (Unstressed and Stressed) or day 20 (Unstressed and Stressed + Recovery). Isolated whole bladder studies were used to assess compliance, urothelial mediator release and contractile responses. Exposure to stress increased plasma corticosterone levels almost three-fold (P<0.05) but this returned to baseline during the recovery period. Contractile responses of the bladder to carbachol and KCl were also increased following stress, and again fully recovered after a 10-day stress-free period. In contrast, stress increased urinary frequency four-fold (P<0.001), but this did not return fully to baseline during the recovery period. Bladder compliance was unchanged by stress; however, it was increased in the stressed + recovery group (P<0.05). Thus, following a stress-free period there is partial recovery of voiding behaviour, with an increase in bladder compliance possibly contributing to the compensatory mechanisms.
心理应激会导致人类和啮齿动物模型的膀胱功能障碍，在反复暴露于环境应激后，尿频率增加和收缩反应改变。然而，在去除应激源后这些变化是否持续尚不清楚，本研究旨在确定在去除应激源后，排尿行为和膀胱功能的应激诱导变化是否恢复。成年雌性小鼠被分配到三个组：未应激组、应激组或应激+恢复组。应激组的动物每天接受 1 小时的水回避应激，未应激组的动物年龄匹配并在正常条件下饲养。对于恢复研究，动物在没有应激暴露的情况下再饲养 10 天。定期评估排尿行为，并在第 10 天（未应激和应激）或第 20 天（未应激和应激+恢复）处死动物。进行离体全膀胱研究以评估顺应性、尿路上皮介质释放和收缩反应。应激导致血浆皮质酮水平升高近三倍（P<0.05），但在恢复期间恢复到基线。应激后膀胱对卡巴胆碱和 KCl 的收缩反应也增加，在 10 天无应激期后完全恢复。相比之下，应激使尿频率增加了四倍（P<0.001），但在恢复期间并未完全恢复到基线。应激对膀胱顺应性没有影响；然而，在应激+恢复组中，膀胱顺应性增加（P<0.05）。因此，在无应激期后，排尿行为有部分恢复，膀胱顺应性增加可能有助于代偿机制。
