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

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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.