Last week, Professor of urology, Chris Chapple had a review published in Continence, titled
“The sensory system is a target for pharmaceutical therapy of overactive bladder.” https://search.app/9amBeV5vb5EWtVMp7
In it he states, “Traditionally, it has been assumed that the target for treating the storage symptoms of OAB is the detrusor muscle.“ and also “There is now increasing evidence that there is the release of neuroeffector agents, such as acetylcholine, nitric oxide and ATP, from the mucosa (in particular, the urothelium), especially when put under mechanical stress. The urothelium is therefore able to respond to a wide variety of mechanical stresses during bladder filling and emptying. It has been reported that the magnitude of neurotransmitter release, such as acetylcholine and ATP, is increased and may play an important role in patients with lower urinary tract dysfunction, such as OAB” and then, “It seems likely that anticholinergic therapy is likely to additionally exert a direct effect on afferent neurotransmission. This is not a surprising conclusion, as the pivotal symptom of OAB is urgency. This raises the question of whether the widely held view that the main target of all therapy must be the detrusor muscle and its cholinergic innervation is entirely correct.”
His conclusion includes, “The evidence provided here would support the hypothesis that the detrusor muscle is not the primary target for the effective clinical therapy of OAB. An important mode of action for effective therapy is likely to be via modulation of the sensory traffic to the brain, affecting the perceived sensory symptom of urgency and, hence, OAB.”
With classical British understatement, he indicates that, for decades, we’ve been directing pharmacotherapy for urinary urgency (OAB and NLUTS) at the wrong targets (detrusor) when we should have been aiming squarely and directly at urothelial afferents.
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