Can modulation of oxidative stress in the brain be a breakthrough treatment for lower urinary tract symptoms?

我们在代谢综合征（MetS）或盐负荷高血压（HT）大鼠模型中研究了MetS或HT对膀胱功能、血流量和上皮介质相关变化的影响。这些模型表现出频繁的排尿。膀胱上皮细胞释放的ATP、PGE2和NGF的量显著增加。血流量的显著减少伴随着氧化应激的增加。血管紧张素II受体阻滞剂（ARB）和α 1A阻滞剂增加血流量，降低MetS膀胱的氧化应激，从而抑制逼尿肌过度活动。ARB治疗的男性HT患者的下尿路症状评分较低。膀胱缺血和伴随的氧化应激通过增加膀胱上皮细胞释放ATP、PGE2和NGF，在MetS和HT储存功能障碍的发展中发挥重要作用。增加血液供应的药物可通过抑制氧化应激来改善排尿反射。

We investigated,in rat models of metabolic syndrome (MetS) or salt-loading hypertension (HT),effects of MetS or HT on bladder function,associated changes in blood flow and epithelial mediators. These models showed frequent micturition. Amounts of ATP,PGE2 and NGF released from the stretched bladder epithelium were significantly increased. A significant decrease in blood flow was concomitant with increased oxidative stress. Angiotensin-II receptor blocker (ARB) and alpha1A blocker increased blood flow and decreased oxidative stress in the MetS bladder,resulting in suppression of detrusor overactivity. Score of lower urinary symptoms was found to be lower in male HT patients treated with ARB.Bladder ischemia and concomitant oxidative stress play an important role in development of storage dysfunction in MetS and HT via increases in release of ATP,PGE2 and NGF from the bladder epithelium. Agents increasing blood supply may improve micturition reflex via suppression of oxidative stress.