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Update on Uropharmacology: Bladder Dysfunction, Nitric Oxide, and Reactive Oxygen Species

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Abstract

The role of nitric oxide (NO) in the pathophysiology of lower urinary tract symptoms (LUTS), detrusor overactivity (DO), and overactive bladder symptoms does not seem to be established. As demonstrated in animal models, interference with the NO/cyclic guanosine monophosphate (cGMP)/cGMP-dependent protein kinase (PKG) pathway at any level (NO synthesis, soluble guanylate cyclase, cGMP, PKG) will lead to DO. One important factor influencing the bladder NO/cGMP/PKG pathway is oxidative stress, in which an abnormal level of reactive oxygen species (ROS) causes tissue damage. ROS may be involved in several bladder pathologies known to show LUTS/DO in animal models, including bladder outlet obstruction, ischemia/reperfusion, and inflammation. The role of ROS in the generation of storage LUTS (including overactive bladder), has not been clarified, though it seems to involve the NO/cGMP/PKG pathway and other mechanisms. To gain further insights into this important field of investigation, new animal models are required to define potential targets for future therapeutic interventions.

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Andersson, KE., Fullhase, C., Soler, R. et al. Update on Uropharmacology: Bladder Dysfunction, Nitric Oxide, and Reactive Oxygen Species. Curr Bladder Dysfunct Rep 5, 150–156 (2010). https://doi.org/10.1007/s11884-010-0057-4

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